Trauma

General points

• Mechanism of injury is important and must be sought out as they produce typical injury
pattern, these can produce both overtly apparent and covert injuries because of distal
transmission of injuring force:
Injuries Overt Covert
Car dashboard injuries Knee injuries Posterior hip dislocation
Seatbelt injuries Overt abdominal bruising & Mesentery, intestinal,
Vertebral chance fractures duodenal or pancreatic
injuries
Penetrative limb injury Incisional wound Joint capsule penetration
(tested by extravasation of
Saline from intrarticular wound
upon injecting it inside) or
blood vessel rupture
Electrocution Burn injuries Posterior shoulder dislocation
Left sided vehicular impact Lateral compression of pelvies Splenic rupture
High velocity (>2000ft/s) bullet Gunshot entry and exit wound Cavitations internally aside
injury from obvious external wound,
these cavity may be permanent
or temporary (latter exceeds
boundary of visible injury)
Blunt trauma to abdomen Bruises or lacerations over Duodenal, pancreatic injury,
abdomen, Intrabdominal bleed, diaphgramatic rupture, distal
solid organ injruies, hollow esophageal rupture, cardiac
organ rupture valve injury (from back
pressure to heart via abdominal
aorta)
Oblique force to shoulder from Posterior clavicle dislocation or Airway compression, DVT
behind fracture from brachiocephalic vein
compression

• Patient factors: Different age groups are prone to different types of injury owing to
differences in their body composition as follows:
◦ Fall on outstretched hand (FOOSH) injuries: in adults it cause radius fracture, in children
it can cause torus/buckle fracture & monteggia fracture and in elderly it can cause
◦ Abuse: Children and elderly are prone to abuse, look for inconsistent history, multiple
injuries of different ages, finger bruises in child, long bone fracture in pre ambulatory
child and posterior rib fractures.
◦ Femur fracture in healthy adult: Neoplasia or any pathological weakness of bone.
◦ Femur fracture in elderly: Can be due to fall from underlying TIA or arrythmia.
• When patient 1st enters Primary survey is the most initial and important thing to do.
• Generally the adage in injury management is based on hemodynamic stability (BP >90/60,
no skin mottling, cooling etc.).
◦ Hemodynamically stable patient can undergo further investigations like CT
 ◦ Hemodynamically unstable patients should undergo resuscitation, manage life
threatening conditions found on primary survey or sent to OR for exploratory
procedures (e.g laparotomy or thoracotomy).
• The torso is divided into compartments separated by anatomic junctions when the injury
occurs at these junctions or across it then both compartments on either side needs
consideration:
◦ B/w root of neck and thorax or at thoracic inlet: Injury to upper mediastinal structures,
injury to major vessels.
◦ At the level of nipple line (4th intercostal space) junction b/w thorax and abdomen:
Injury to diaphragm, lungs or abdominal solid and hollow viscus organs.
◦ At the level of illiac crest, b/w abdomen and pelvis.

Primary survey
Airway, Breathing, circulation, disability and expsoure, so Called ABCDEs are assessed, among
these any conditions harming ABCs are treated 1st priority before other accompanying injuries.

Airway and Spine stabilization.

• Best assessed by patient’s ability to vocalize; which if present r/o inpatent airway.
• If no h/o vocalization, then, Agitation (s/o hypoxia), Obtundation (s/o hypercarbia),
Presence of tachypnea and respiratory distress (grunting, using accessory muscles for
respiration, Rapid shallow breathing), Cyanosis (although late feature of hypoxia) also
suggests airway Inpatency. Noisy breathing also suggests obstruction, Gurgling, snoring or
stridor suggests obstruction at pharynx or larynx, Hoarseness Implies functional laryngeal
obstruction.
• Simple measures to clear airway includes airway suction & aspiration, jaw thrust and chin
lift, if airway still compromised after these manoeuvrers then oropharyngeal (guedel) or
nasopharyngeal airways are used. Guedel airawy should not be used in children as rotating it
180 degrees after placing it with tube part towards the palate might lead to damage to
pharynx. Any airway inserted through the nose is to be avoided in Cribriform plate fracture
as the tube may pass through the cranial vault.
• When in doubt intubate.
• Indications for Intubation:
◦ Inpatent airway
◦ Inability to maintain oxygenation by face mask supplementation or the presence of
apnea.
◦ H/o Inhalational injury (e.g pt enclosed in house fire), O/E signed facial hair, sooty
sputum, laryngoscopy showing burned mucosa, edema of oro/nasopharynx- burns
gradually lead to progressive edema of upper airways ending in their obstruction hence
intubation in anticipation of that is required as it becomes difficult once edema sets in.
◦ Maxillofacial injury: Leads to development of edema around upper airway
◦ In penetrative neck injury or tracheal/laryngeal fracture if hard signs of vascular or
aerodigestive injuries are present like expanding hematoma, subcutaneous emphysema,
food content spilling out of neck injury , audible noisy breathing, stridor or hoarseness.
◦ Patient unconscious on arrival or GCS <8
◦ Patient had seizure on arrival.
◦ Agitated patient.
◦ Potential for aspiration from blood or vomitus (e.g in upper GI bleed causing large
hematemesis)
• Intubation is done using definitive airway which can be of 2 types non surgical or surgical.
Non surgical airways include Nasotracheal or orotracheal airways, these are cuffed at ends
 which can be inflated to form a lock inside cricoid. Cuff is not inflated in pediatric because
their cricoid ring forms a natural lock around uncuffed ET tube, cuff inflation if done should
have their pressure measured, with <30mmhg being considered safe.
• If Intubation fails then laryngeal mask airway is used temporarily before attempting with
fiberoptic intubation or surgical airway.
• Surgical airway involves needle cricothyroidotomy or surgical cricothyroidotomy. Needle
cricothyroidotomy is used in pediatric, surgical is contraindicated (because of damage to
cricoid cartilage, the only circumferential support to upper trachea).
• Meanwhile cervical spine is protected by Cervical collar or board, in cases where it needs to
be removed (examination, investigations etc.) then patients head is stabilized by one person
and other teammembers log roll the patient.
Breathing and Ventilation
• Assess for any chest deformities on palpation, asymmetric chest movements, lack of breath
sounds, tracheal position and Jugular venous distention.
• Pneumothorax, Massive hemothorax, flail chest with contusion identified in primary survey
are treated there itself.
• Auscultate high anterior chest wall for pneumothorax and posterior chest wall for
hemothorax.
• Pneumothorax can be simple,open and tension types:
◦ Simple should be treated before starting PEEP ventilation as it can turn into tension
pneumothorax.
◦ Tension pneumothorax acts as a one way valve for air hence air rapidly accumulates and
compresses the mediastinal structure requiring urgent treatment.
◦ Open pneumothorax acts as a sucking chest wound continuously accumulating air.
◦ O/E pts have absent breath sounds, jugular venous distension and deviated trachea, latter
two are not present always.
◦ Tamponade can also cause dyspnea and JVD and it can be differentiated from
pneumothorax by presence of breath breath sounds on auscultation. Tamponade also has
distant heart sounds and decreased pulse pressure.
◦ Initial management of pneumothorax is needle thoracotomy and later placing a chest
tube. Open chest wound is managed by 3 sided dressing and a chest tube insertion
• Massive hemothorax:
◦ It is suggested by O/E finding of dullness on percussion, absent breath sounds, tracheal
shift, low BP not responding to fluid resuscitation and if chest tube already in place then
initial/rapid output of >1500ml of blood or 200-300ml/hr output for 2-4 hours.
◦ Front and back side of chest should be auscultated because lungs float over blood in
hemothorax so on front side breath sounds can be heard but in back it cannot.
◦ Initial Management is immediate chest tube placement and if bleeding uncontrolled then
emergency thoracotomy and controlling intercostal vessel haemorrhage.
• Flail chest causes severe pain to patient leading to voluntary splinting of chest affecting
ventilation and oxygenation, ample analgesia should be given in such case to facilitate
appropriate oxygenation and ventilation.
Circulation
• Shock is the most important condition to be managed. It is a circulatory system abnormality
leading to inadequate tissue perfusion & oxygenation.
• 1st step is to recognize the presence of shock
◦ Assess for shock in the patient most IMP. Critical findings yielding important
information in seconds can be:
▪ Level of consciousness: Patient with loss of consciousness in absence of obvious
head injury is most likely due to shock.
▪ Skin perfusion: Presence of skin pallor or ashen gray look, coolness or mottling
are grave signs of hypovolemic shock. Warm pink extremities are sign of perfusion.
 ▪ Characteristics of pulse: Rapid, thready pulse and worse still, one not
peripherally palpable is a grave sign of shock. Slow, regular and full pulses are
usually a sign of normovolemia.
◦ Any injured patient who is cool touch and tachycardic should be considered in shock,
until proven otherwise.
◦ Narrow pulse pressure is also an early sign of shock. And it is a useful measure in
elderly patients who may not exhibit tachycardia due to limited cardiac response to
catecholamines or concurrent used of beta blockers.
◦ Although hypotension is found in shock it appears way later after shock sets in and so
shock may be missed by depending a lot on that finding.
◦ Base deficit or lactate levels are useful to determine presence of shock and its severity,
serial measurements are useful to measure patient’s response to treatment.
◦ Patients in advance age have poor cardiac contractility, poor catecholamine
responsiveness and on drugs that affect the former like beta blockers hence they may
present in shock with normal vitals (e.g SBP of 100mmhg), also many have
Atherosclerotic vascular disease which makes organs sensitive to even slight reduction
in oxygen, hence advanced monitoring should be started early in these cases.
◦ Atheletes have increased physiologic reserves (CO, blood volume) and resting
bradycardia hence they may present normally even in shock
◦ Pregnant patients also have large blood volume and mother may be asympotomatic
while in shock, but there will be fetal distress from decreased perfusion.
◦ Pacemaker using patients cannot increase rate physiologically, thus they need advanced
monitoring to guide fluid replacement and their pacemaker rate is changed accordingly.
• Most of the cause of shock are due to hemorrhage/hypovolemia & is managed as as such
unless proven otherwise, however a small number of cases occur due to non-hemorrhagic
conditions like tension pneumothorax, cardiac tamponade, neurogenic, cardiac failure or
from sepsis even without considerable hemorrhage the shock due to latter category
conditions may temporarily improve from volume resuscitation.
◦ Cardio failure causes a specific type of shock called cardiogenic shock. Cardiac failure
can occur from Blunt cardiac injury(rapid deceleration injury), tamponade, air embolism
or rarely MI (cocaine users or elderly).
◦ Tamponade occurs most commonly from penetrative injury but can also happen with
blunt injury.
◦ Tension pneumothorax occurs with penetrative wound.
◦ Neurogenic shock:
▪ Isolated intracranial injury do not cause neurogenic shock unless brain stem is
injured.
▪ Cervical & upper thoracic spinal cord injury produce hypotension due to losss of
sympathetic tone compounding the effect of hypovolemia caused by trauma which
also compounds effect of neurogenic shock by causing sympathetic denervation.
▪ Classical presentation is Hypotension without tachycardia or cutaneous
vasoconstriction, a narrowed pulse pressure is not seen in neurogenic shock.
• Basic principles behind Haemorrhagic shock management are restoring venous return to
normal by locating and stopping source of bleeding, Volume repletion will allow recovery
from shock status only when bleeding has stopped, hence Definitive control of haemorrhage
& restoration of adequate circulating volume are goals of treating haemorrhagic shock.
• 1st step in shock management is crystalloid fluid resuscitation via 2 large bore, short,
peripheral IV cannula, an intra-osseous needle or central venous catheter. 1L of RL/NS is
given. Patients who fail to respond to crystalloid resuscitation (non responders) should
receive blood product resuscitation because >1.5L of crystalloid increases risk of death from
coagulopathy.
 ◦ Response is checked measured by urine output, clinical indicators of BP, pulse pressure,
skin condition are only qualitative indicators. Based on the response further management
is indicated:
▪ Responders: Those patients who normalize with fluid bolus and do not have
hemodynamic deterioration with maintenance fluid. Can be safely managed with
only crystalloids.
▪ Transient responders: Those patients who normalize with fluid bolus but have
worsening of hemodynamic status when shifted to maintenance fluids, these patients
have blood loss of 15-40% of their blood volume and need blood product transfusion
with operative or angiographic control of bleeding sites, if there is transient response
even to blood products, then Massive transfusion protocol (MTP) and Urgent
exploration is required.
▪ Non responders: did not respond to either crystalloids or blood, next step is emergent
angioembolization or operative control of bleeding with MTP. Non haemorrhagic
causes of shock as mentioned above should also be considered and managed.
Cardiac ultrasound to monitor and detect type of shock.
◦ In shock BP should not be used as a measure of response because in shock we aim to
restore tissue perfusion and oxygenation that depends on Cardiac output, hence we aim
to increase cardiac output, because MAP=TPR X CO, BP can also rise with conditions
increasing TPR for e.g with Vasopressor use, hence raised BP being falsely correlated
with improvement of shock.
• After patient is stabilized next step is to assess the source of bleeding which can be external
or internal:
◦ External sources: Large open wounds, long bone fractures, exsanguinating amputated
limb. Rapid external blood loss is managed by Direct manual pressure, Tourniquets
can be applied in case of massive exsanguination or when direct pressure is not
effective.
◦ Internal sources: 5 major body compartments are involved in hemorrhage, which are
Thorax, abdomen, Pelvis, Long bones and Retroperitoneum. Physical examinations and
imaging can confirm the source of bleeding.
▪ Hemothorax can be seen on CXR, requires chest tube placement, if output is rapid
accumulation of >1500ml of blood or rate is 200-300ml/hr of blood for 2-4 hrs then
emergency thoracotomy is required, in which intercostal and intramammary arteries
are ligated.
▪ Intraperitoneal accumulation of blood can be seen in FAST, if present then needs
emergency laparotomy for exploration, whoever in pediatrics small intraperiotneal
fluid is a common finding for any abdominal trauma and does not require surgical
exploration.
▪ For Pelvic fractures a pelvic film quickly identifies fracture and a pelvic binder is
worn to control bleed f/b operative or angiographic treatment for embolization for
arterial hemorrhage.
▪ For long bone fractures splinting & direct pressure application is done.
• Gastric dilation is often required esp. In children, because it cna cause unexplained
hypotension or cardiac dysrythmia, usually bradycardia from excessive stimulation.
Disability (Neurologic evaluation)
• Pupillary size and GCS are IMP. Findings needed to be evaluated.
◦ Pupillary size suggests injury level and lateralization.
◦ Low GCS esp. <8 suggests Brain injury and its motor component is an IMP. Prognostic
feature. A baseline should be taken before administering sedatives.
• Altered level of consciousness suggests brain injury which can happen from Hypoxia,
hypovolemia, hypoglycemia, direct injury or substance use. Hence it presence drives the
need to reevaluated ventilation, oxygenation and circulation status of patient.
 • Evaluate for neurogenic shock, classically due to cervical or high thoracic spinal cord
injury. It presents O/E as hypotension and inability to move extremities, if patient can move
upper extremity then it can be ruled out. It is managed by Vasopressors in contrast to other
types of shock requiring fluid resuscitation.
Exposure & Environmental control
• Patient fully exposed top-down and examined for injuries, presence of chemicals, if h/o
chemical exposure then the patient is sprayed with water and all possible contaminated
clothes are carefully quarantined.
• Temperature control is essential, patient frequently become hypothermic during examination
in emergency room, warm blankets, external warming device may be used, in severe cases
warm IV saline is administered.
Adjuncts to primary survery:
• ECG for arrythmias,
• pulse oximetry and ABG for oxygen saturation and carbon monoxide levels,
• capnometry for ventilation monitoring,
• Urinary catheter to measure output which is used to evaluate patient volume status, renal
perfusion and reliving retention and
• Gastric catheter for decompression, checking for bleed, decreasing aspiration and for enteral
nutrition:
◦ In unconscious patients gastric distension increases risk of aspiration
◦ In patients with cribriform plate fracture nasal insertion of ryle’s tube is avoided as it can
enter inside cranium, in these cases oral insertion is done.

Secondary Survey
Detailed h/o allergies, past illness, medications, current pregnancy & events around injury with
possible mechanisms are taken. Head to toe examination for obvious and possibly hidden injuries
are performed.

Head
• IMP. To identify all neurological injuries.
• Whole scalp and head surface should be evaluated for lacerations, contusions and fractures.
• Scalp lacerations bleed profusely and may lead patient into shock hence its control is urgent.
• Eyes should be examined ASAP as edema may develop later making further examination
difficult, importantly pupillary reflex & visual acuity other findings to remain alert for are
haemorrhage of conjunctiva or fundi, penetrating injuries, lens dislocation & ocular
entrapment.
◦ Visual acuity can be assessed by handheld Snellen’s chart or asking patient to read the
fine print.
◦ Ocular mobility should be evaluated to r/o entrapment from orbital fractures.
• Maxillofacial structures can be examined by palpable step offs at nose, zygoma, ear,
mandible & mouth, intraoral examination, assessment of occlusion & assessment of soft
tissues. Any midface injuries can compromise airway requiring urgent airway placement.
Maxillofacial injuries without airway compromise or massive hemorrhage should be treated
only when the patient is stabilized.
Cervical spine and neck
• Patients with maxillofacial or head injury also likely have cervical spine injury.
• Patients with normal neurologic examination does not r/o cervical spine injury.
• Cervical spine injuries are cleared clinically and radiographically by certain established
criterias like NEXUS or Candaian C spine rule.
 • Assess for tracheal deviation, laryngeal fractures, subcutaneous emphysema, cervical spine
tenderness, palpable step offs, hematomas and crepitus. Vessels should be auscultated for
presence of any bruits.
• Any protective helmet should be removed and cervical collar be placed.
• Penetrating neck injuries should evaluated if it extends through the platysma, such injuries
should not be probed or explored without surgical consult.
• Expanding hematomas, arterial bruits or airway compromise requires urgent surgical consult
• Unexplained or isolated paralysis of upper extremity raises concerns for cervical nerve root
injury.
Thorax
• Most of it done in primary survey, same should be repeated here.
• Entire chest cage should be palpated including clavicles, sternum & ribs.
• Sternal pressure eliciting pain is s/o sternal fracture of costochondral separation.
Abdomen & pelvis
• Normal initial examination as done in primary survey does not rule out Intrabdominal
injuries. Close observation and frequent reevaluation of the abdomen is required, as over
time the abdominal findings change.
• Ecchymosis over illiac wings, labia, scrotum or pubis suggests pelvic fractures.
• Pelvic ring palpation should be done to elicit pain in alert patients.
Perineum rectum & vagina
• Perineum assessed for contusions, lacerations & urethral bleeding which suggests pelvic
fracture.
• Rectum should be assess for bleeding and integrity of its wall which becomes compromised
with displaced pelvic fractures.
• Palpation of prostate gland is not reliable sign of urethral injury.
• Vaginal examination for vaginal lacerations should be performed that can happen with
displaced pelvic fractures.
• Pregnancy test in all childbearing aged females.
Musculoskeletal
• Assess for contusions, lacerations and tenderness over extremities.
• Significant signs O/E may be present in absence of evident fracture on X-ray from
ligamentous or tendon injuries.
• Ligament injuries produce joint instability.
• Muscle tendon rupture interferes with active motion of affected structure.
• Back examination is essential before concluding the survey as it is frequently missed and
and there could be significant injuries.
Neurologic
• Motor and sensory evaluation of extremities should be performed, patient’s level of
consciousness need to be re-evaluated as well as pupillary size and response. GCS score can
detect early changes.

Thorax
• Injuries can be direct or iatrogenic from central line placement or esophageal endoscopy.
• Most of these injuries cause Hypoxia, Hypercarbia & acidosis that requires management of
vitals. Most of these problems are found out in primary survey and manage there itself with
simple measures like airway control or decompression with needle, fingers or chest tube.
• Life threatening injuries: Diagnosis of most of these are covered in primary survey notes,
here management is given.
◦ Airway problems:
 ▪ Airway obstruction: Can occur with:
Swelling of the airway.
Aspiration of blood & vomitus.
laryngeal injury from direct trauma or indirectly by shoulder restraint misplaced to
neck.
Posterior dislocation or fracture of clavicular head at sternoclavicular junction.

Patients have e/o air hunger, O/E they have intercostal and sternoclavicular muscle
retractions. e/o of foreign body may be found on oropharynx inspection, diminished
air movement may be heard near nose, mouth or auscultation of lung fields, stridor
or changes in voice quality may be present, crepitus may be felt over the anterior
neck & defect may be palpable over the sternoclavicular joint.

Tt: Suctioning of the aspirated blood or vomitus, placement of definitive airway.

Reducing posterior dislocation of clavicle by abducting the shoulder and providing
traction and then applying extension force on the shoulder or by grasping the clavicle
with a penetrating towel clamp.
▪ Tracheobronchial tree injury: Can be caused by deceleration from blunt injuries,
blast injuries and penetrating injuries, these work to shear the airway at a point of
attachment from where it is mobile.

Patients presents depending on location of injury generally with hemoptysis,

cyanosis, tension pneumothorax, cervical subcutaneous emphysema. Proximal
injuries of trachea or mainstem bronchi results in large amount of
pneumomediastinum, whereas distal airway involvement causes recurrent
pneumothorax with air leak. Incomplete expansion of lung and large air leak when
placing chest tube suggests this type of injury and is confirmed with bronchoscopy.

Treatment requires immediate airway placement often with help of fiberoptics

because of anatomical deformities accompanying such type of injuries, urgent
surgical consultation to be done.
◦ Breathing problems:
▪ Tension pneumothorax: Managed by needle decompression by placing a cannula at
2nd intercostal space at mid-axillary line followed by placing a chest tube at safety
triangle at 5th intercostal space.
▪ Open pneumothorax: Caused by open chest wound with diameter greater than
2/3rds of trachea. It presents with signs of pain, difficulty breathing, tachypnea,
decreased breath sounds & noisy movement of air through the chest wall injury.

Tt: Close the wound with sterile dressing large enough to overlap the wound’s edges
which is taped securely on its 3 sides to provide a flutter valve effect f/b by placing a
chest tube at place remote from the original wound.
▪ Massive hemothorax: Fluid resuscitation f/b Placing a chest tube f/b surgical
consult to ligate bleeding vessels.
◦ Circulatory problems
▪ Cardiac tamponade: Fluid resuscitation to increase cardiac output f/b subxiphoid
pericardiotomy. Pericardiocentesis is not effective because most cases of tamponade
happen due to dry clot.
▪ Traumatic cardiac arrest: Occurs from 5Hs and 5Ts, managed according to ACLS
protocol.
• Potentially life threatening:
◦ Simple pneumothorax: Diagnosed by upright X-ray, small and asymptomatic
pneumothorax can be managed with aspiration otherwise it is typically managed with
chest tube insertion at 5th intercostal space.
◦ Flail chest and pulmonary contusion: Flail chest happens when there is fracture of 2
or more contiguous ribs at 2 or more areas of the bone, it can also happen when there is
costochondral separation of single rib, this leads to paradoxical motion of chest wall and
voluntary splinting causing poor respiratory effort & limit chest wall movement.
Pulmonary contusion is bruising over lung leading to accumulation of blood and fluids
at injury site hampering oxygenation and ventilation. Flail chests are a/w pulmonary
contusion and the latter causes greatest physiological insult in form of mortality from
respiratory failure due to ARDS or pneumonia. Pulmonary contusion can be detected on
CT/X-ray as higher higher density opacity in vicinity of chest injury, which may cross
fissures, although they may not appear early on imaging and develop within 24-48
hours, if present early signify severe case which often rapidly progress to respiratory
failure. Combination of these 2 causes hypoxia & hypoventilation necessitating
intubation (esp. If hypoxic or comorbid status like COPD or renal failure), fluid
resuscitation if hypotensive otherwise not as it may cause volume overload. Analgesic is
necessary to improve respiratory effort in flail chest. Mild pulmonary contusion is
managed by oxygenation, aggressive pulmonary toileting and analgesia, mechanical
ventilation may be needed for severe case.
◦ Blunt cardiac injury: Caused Most commonly by moto vehicle accidents & falls. Blunt
injury to heart causes myocardial contusion, cardiac chamber rupture, coronary artery
dissection/ thrombosis or cardiac tamponade. The condition may be confounded by chest
musculoskeletal injuries and it can only ever be truly confirmed on direct inspection of
heart, it is suggested be features of hypotension, dysrythmia, wall motion abnormality on
2D-echo or ECG abnormalities typical of MI, multiple PVCs, unexplained sinus
tachycardia, A-fib, Bundle branch blocks or ST changes. Elevated CVP might suggest
right chamber injuries. Patients require 24 hour ECG monitoring because risk of
arrythmia decreases substantially over 24 hours.
◦ Traumatic aortic rupture: Caused by deceleration injuries like motor vehicle accidents
or falls. Most survivor cases have haemorrhage contained by adventitia layer or the
surrounding anatomy e.g mediastinum with the best prognosis for tears near ligamentum
arteriosum, free rupture of aorta is usually fatal, hence hypotension is attributed to
unidentified bleeder. Specific signs and symptoms are widened pulse pressure,
asymmetric BP but frequently absent hence diagnosis based on mechanism of injury and
radiographic features like widened mediastinum, absent aortic knob, elevated right
mainstem bronchus & depressed left bronchus, shifted mediastinum to right, absent
space b/w pulmonary artery and aorta, deviated esophagus to right, fracture of 1st and 2nd
rib/scapula & left hemothorax. Helical CT is best for Dx, otherwise CT aortography and
transesophageal echo can be substitue. Management involves Decreasing heart rate with
beta blockers like esmolol or CCBs like nicardipine. Endovascular repair by CTVS is
defintive treatment.
◦ Traumatic diaphragmatic rupture: Most cases caused by blunt trauma producing
radial tears, penetrating injuries produce only small defect which are asymptomatic.
Right sided diaphragmatic defects are less severe from occlusion be liver. It is suggested
on Chest X-ray showing elevated diaphragm on the right and gastric contents in left
chest. Left sided rupture can be confirmed by passing a nasogastric tube f/b X-ray which
shows the tube in left thorax. Presence of peritoneal lavage fluids in NG tube after DPL
also confirms it. Tt is direct repair. Placing a chest tube may injure abdominal contents.
◦ Blunt esophageal injury: Most commonly caused by penetrating injury and rarely by
blunt injury due to expulsion of gastric contents into lower esophagus producing linear
tears. Such injuries leak into mediastinum causing mediastinitis which may rupture into
 pleura causing empyema. Presentation is similar to boerhave or mallory weiss syndrome
with chest pain radiating to back or upper abdomen pain, odynophagia, dysphagia,
hematemesis & subcutenous or mediastinal emphysema. The setting is typically a patient
with a left hemothorax or pneumothorax without a rib fracture who has received a severe
blow to epigastrium or lower sternum and is in pain or shock out of proportion to
apparent injury. Particulate matter may begin to drain out of chest tube once blood
clears, presence of leakage of contrast material & mediastinal air from esophagography
(water soluble f/b thin barium, helical CT esophagography > fluroscopic esophagram) or
disruption of mucosa on esophagoscopy confirms diagnosis. Tt is wide drainage of
mediastinum and pleura f/b direct repair.
• Thoracotomy is indicated in:
◦ Control of intrathoracic hemorrhage
◦ Control of massive air leak
◦ Internal cardiac massage in case of arrest post elective CTVS surgeries.
• Emergency department thoracotomy is considered futile if
◦ CPR >10 minutes or CPR >5 minutes without intubation.
◦ Blunt trauma cases with no signs of life at scene of injury.

ABDOMEN
General points
• Injury to thorax below nipple line should also have suspicion for abdominal injury.
• Significant haemorrhage into abdominal compartment may not cause peritoneal irritation or
change in any dimension.
• Air bag deployment does not protect abdominal injury.
• Peritoneal irritation occurs from blood and hollow viscus content leakage.
• Most common involved organ in Blunt trauma is Spleen> Liver> Small bowel
>retroperitoneum.
• Most common involved organ in penetrating are Liver> Small bowel>Diaphragm>colon its
subtype gunshot wounds involves small bowel>colon>liver> Vasculature
• No correlation with bowel sounds and abdominal injury.
• Signs of peritoneal irritation (rebound tenderness: slight peritoneum movement on
percussion & involuntary guarding) or low BP not responding to fluids require urgent
surgical exploration.
• Examine skin folds in obese patients as they frequently mask injuries.
• Instability of pelvis is suggested by picture of pelvic fracture and hypotension. Pelvic
fracture is suggested by ruptured urethra (scrotal hematoma or blood at meatus), limb
discrepancy, rotational deformity without obvious fracture. In such cases pelvis is not
manipulated due to fear of dislodging a clot restarting bleeding, only gentle palpation is
done to identify tenderness. Mechanically unstable pelvis travels cephalad due to muscular
forces and externally rotates outwards from effect of gravity, this expands the volume pelvis
compartment accomadating greater volumes of blood, pelvic binders are worn to limit this
expansion.
• Pelvic binders worn over greater trochanters not illiac crest.
• In unresponsive menstruating women any tampons should be removed as they cause delayed
sepsis.
• Gastric catheter used to decompress GI and to reduce risk of aspiration. Presence of blood in
GI contents suggests bleeding from esophagus or upper GI tract.
• Urinary catheter is placed to reduce retention, monitor output, and identify bleeding. It
should not be placed before FAST is complete because FAST visualizes organs best when
full bladder, it should also not be placed in any signs of Genitourinary injury like hematuria,
pelvic fracture requiring binder, blood through urethral meatus, inability to void, scrotal
hematoma or perineal ecchymosis without 1st confirming intact genitourinary tract by
retrograde urethrogram.
• FAST is done bedside and any presence of free fluid in abdomen needs laparotomy.
• CT consumes time hence cannot be done for unstable patients. It can detect injuries to
retroperitoneum and pelvic organs undetected by FAST, presence of free fluid in abdomen
suggests injury to GI tract and/or its mesentry
• Diagnostic peritoneal lavage, performed when FAST or CT unavailable. Most useful for
unstable blunt trauma or multiple cavitary or tangential penetrating injuries. Its performed
by operating surgeon. Requires gastric and urinary decompression beforehand. It is avoided
in advanced cirrhotics, coagulopathics, morbidly obese & previously abdominally operated.
Aspiration of gastric contents, vegetable fibers or bile mandates exploration & the same if
>10cc (>100,000 RBCs or >500WBCs ) or more blood aspirated in unstable patient.
Specific injuries

Penetrating abdominal wound

• Anterior abdomen:
◦ Patients who are unstable, bowel or omental evisceration or peritoneal signs are referred
for urgent exploration
 ◦ Patients with anterior abdomen stab wounds can undergo local wound exploration to
determine if peritoneum is intact. Presence of any defect in anterior rectus fascia
suggests peritoneum is not intact and patient can undergo either CT imaging, diagnostic
laparoscopy or Laparotomy.
• Flan or back:
◦ Injuries can be suspected reliably based on serial examination showing signs of
peritonitis or CT.
Duodenal Injuries: Occurs in unrestrained drivers or direct blow to abdomen such as from bicycle
handlebars. Bloody gastric aspirate or retroperitoneal air on CT or abdominal radiograph suggests
such injury. An upper GI X-ray series, double contrast CT or emergent laparotomy is indicated for
high risk patients.:
• Duodenal hematoma gets resolved on its own and its only an issue if it leads to gastric outlet
obstruction, which can be managed by gastric decompression, initiation of total parenteral
nutrition & reevaluation of gastric emptying with contrast study after 5-7 days, if its not
resolved by 14 days then exploration is done to evacuate hematoma, evaluate perforation,
stricture or associated pancreatic injury. Hematomas will decompress when mobilizing
duodenum & any hematomas found incidentally should not be opened unless concern for
full thickness injury.
Pancreatic injury: Occurs with direct blow to epigastrium. Early normal serum amylase levels
does not rule this out and even if elevated may be due to other cause. CT may miss in early injury
period.
Hollow viscus injury: Caused by sudden deceleration producing shearing at a fixed point of
attachment, particularly with improper seat belt positioning. Transverse linear ecchymosis at
epigastrium (seat belt sign) or lumbar chance fracture also suggest intestinal injury.:
• Small bowel injury: Blunt trauma can cause ischaemia and require resection. Hematomas to
be explored for any perforation. Low energy injury can be managed with debridement,
whereas high energy injury require resection with anastomosis.
• Colon: If minimal contamination then colon can be retained, if extensive contamination or
unstable patient or doubtful viability then the colon is removed and closed by forming a
defunctioning colostomy.
Solid organ injury: In unstable patients or those with uncontrolled bleed laparotomy is done
whereas those who are stable can be managed conservatively:
• Liver: Can be injured with blunt or penetrating trauma. Investigation of choice is CT. Stable
patients are managed conservatively whereas unstable patients require laparotomy. In
laparotomy pringle’s manuever (compressing portal tract) is important to control
hemorrhage.
• Biliary tract: Drainage or T-tube repair is done
• Pancreas: Caused by blunt injury. Tail injuries are managed by closed drainage whereas
distal pancreatectomy is done if ducts are involved. Proximal injuries (to the right of
Superior mesentric artery) are treated conservatively. Whipple’s procedure should not be
performed in emergency.
• Most isolated splenic injuries in children can be managed nonoperatively. Splenectomy is
considered when patient has multiple injuries, age >55 or hemodynamic instability.
Head Trauma
General points
• Intracranial haemorrhage never causes shock due to closed nature of such space.
• Due to compression of neurological connective tissues hypoxia and ischemia occurs leading
to secondary injury. Main treatment goal is to reduce such secondary injuries by maintaining
oxygen and BP.
• GCS is the best indicator for severity of brain injury, the motor score is most reliable
predictor of outcomes. GCS Score of 8 or less is generally accepted definition of coma or
severe brain injury.
• Scalp can get lacerated leading to haemorrhage enough to cause hemorrhagic shock (esp. In
child and elder), hence it needs to be repaired 1st.
• Main problem in intracranial haemorrhage is that h due to it occurring in an enclosed
compartments initially displaces blood and CSF and when it cannot be displaced anymore
leads to rapid elevation of Intracranial pressure.
• Maintaining adequate cerebral perfusion is the main treatment goal, which can be done
mainly by decreasing ICP, maintaining adequate intravascular volume and MAP & restoring
adequate oxygenation and ventilation.
• Lesions like haematomas that increase intracranial pressure to be evacuated early.

Injuries
• Skull fracture:
◦ Basilar skull fracture (raccoon’s eye[periocular hemorrhage], Battle’s sign
[retroauricular bruise], CSF rhinorrhea or otorrhea, haemotympanum, CN 7 & 8
dysfunction) require CT for Dx,
◦ Skull fracture near carotid canal requires CT angiography to r/o pseudoaneurysm,
dissection or thrombosis.
◦ Open or compound fracture communicates with scalp laceration when dura is torn
• Intracranial lesions:
◦ Diffuse brain injury: Can happen with concussion presenting as transient non focal
neurological disturbance with LOC or with severe hypoxic injuries that may present on
CT as normal appearence or swollen brain & loss of grey-white matter distinction. In
deceleration or high velocity impact injuries, multiple punctate hemorrhages at gey
white matter junction on CT suggests diffuse axonal injury from shearing.
◦ Focal injuries:
 ▪ Epidural hematoma: from medial meningeal artery tear at pterion, patients have lucid
interval after initial brief LOC and thereafter progressive worsening of neurological
status. On CT it appears as lenticular hemorrhage.
▪ Subdural hemorrhages: Caused by shearing of bridging veins in elderly, producing
hemorrhage that takes shape of brain contour. A/w concomittant parenchymal injury.
▪ Subarachnoid haemorrhage: Due to rupture of berry aneurysms at circle of willis,
infective infiltration of arterial walls (mycotic aneurysm) which may occur after IV
drug use or infective endocarditis or from pseudoaneurysms that develop following
trauma or surgery.
• C/c patient has thunderclap headache, which may be associated most commonly
with vomiting, otherwise with LOC or seizures. Meningeal signs and
photophobia develops over hours. Painful third nerve palsy suggests aneurysm
over posterior communicating artery. Intraocular haemorrhages classically
subhyaloid may be visible on fundoscopy. Combination of subarachnoid
hemorrhage and vitreous hemorrhage is called terson syndrome.

• Investigations:
◦ CT scan most sensitively detect bleed within 1st 12 hours of symptom onset.
◦ CT scan sensitivity worsens after a week of injury, in such cases most
sensitive investigation of choice to detect bleeding is Lumbar puncture &
CSF spectrophotometric investigation for oxyhaemoglobin and bilirubin
levels, these can be detected in CSF, 6-12 hrs after injury but not CSF mixed
with fresh blood from traumatic puncture that is analysed immediately.
◦ If failure of detection in CSF then next best step is cerebral angiography.
• Management: General resucitation measures (ABCDEs), oral nimodipine,
analgesics, laxatives, antiemetics, gastric protection and compressive stockings.
After resuscitation priorities are to stop rebleeding by identifying and closing the
bleeding aneurysm by surgical craniotomy with clipping or endovascular
embolization.
• Complications:
◦ Hydrocephalus: Presents with neurological deterioration after managing
subarachnoid bleeding, most common type of hydrocephalus is
communicating. Needs repeat imaging to confirm.
◦ Delayed ischemic neurologic deficit: Suspected in cases of neurological
deterioration without any CT finding. Cerebral vasospasm is implicated
process. It is managed by maintainging MAP with isotonic fluids and
administration of nimodipine.
◦ Hyponatremia
▪ Contusion and intra-parenchymal injury: Contusions mostly happen on frontal and
perietal areas, and they progress to intra cerebral hemorrhage, hence these cases need
a repeat scan 24 hrs later after the initial scan.
◦ Arterial dissection: May occur spontaneously or in presence of trauma. Dissection can
happen extracranially or at skull base in association with fracture. C/c of headache, neck
pain & focal ischemic defects. Development of delayed deficit esp. In context of skull
base fracture involving carotid canals should prompt urgent CT angiography.
• Complications:
◦ Pituitary and metabolic dysfunction: Electrolyte imbalances lead to brain swelling and
induces seizures, this occurs due to diverse mechanism most importantly cerebral salt
wasting leading to hyponatremia. Pituitary dysfunction causes SIADH leading to
hypervolumic hyonatremia, hyponatremia leads to brain swelling and hence hypotonic
fluids are avoided in such complications.
ADH secretion may be affected leading to diabetes insipidus resulting in hypernatremia
 which may be managed by boluses of desmopressin.
Pituitary hormone levels should be measured.
◦ Seizures: Occurs in TBI especially prone to happen with depressed skull fractures,
presence of ICH & dural tears.
◦ Concussion: Confusion and amnesia are key features, patient may be easily distractable,
forgetful, slow to interact or emotionally labile, gait disturbance and incoordination may
be seen.
◦ Second impact syndrome: Patient with head injury are prone to have a repeat injury the
result of which may form a malignant cerebral edema refractory to treatment, hence
sportsman are advised not to return for play and in case of very severe injury not play for
the whole season.
◦ Post concussive syndrome: It is syndrome that is seen persisting for prolonged periods
after concussion which can also be exacerbated by potential of secondary gains. Patients
may report somatic features like headache, dizziness & disorders of hearing and vision,
they may also suffer a variety of neuro-cognitive and neuropsychological disturbances
like difficulty with concentration and recall, insomnia, emotional lability, fatigue,
depression and personality changes.
Management
• Primary survey:
◦ Airway: Intubation in all comatose.
◦ Breathing: Prevent hypoxia SpO2 >98% are desirable. Prevent hypercapnia and PCO2
>45mmhg, never hyperventilate (<25mmhg) unless acute herniation is suspected
(sudden worsening with FNDs), PCO2 levels around 35 mmhg are ideal.
◦ Circulation: Correct hypotension quickly by establishing euvolemia either with fluid
resuscitation or controlling haemorrhage (SBP in Elder >100 & in young adults >110
mmhg), hypotensive patients are frequently unresponsive to neurological examination.
◦ Disability: Test for GCS and pupillary reflex. Doll’s eyes reflex to be tested only when
cervical spine is clear.
• Initial measures:
◦ Place patient in reverse trendelenberg position by elevating the head by 20-30 degrees.
◦ Loosen the cervical collar to promote venous drainage.
◦ Optimize electrolyte balance and treat hyperglycemia.
• Admission and investigations: Management of head injury beyond primary survey depends
on patient’s GCS score as follows:
◦ Mild injury (GCS 13-15): Patients should have their CT done depending on certain
findings and on fulfillment of certain criteria. Admission depends on presence of CT
findings in these cases.:
▪ When to admit :
• No CT available or abnormal CT
• Focal neurological deficits
• Skull fracture,CSF leak
• GCS did not return to 15 within 2-3 hours
• Suspected intoxication for observation.
• Head CT rules:
◦ Absolute:
▪ All elderly >65
▪ On anticoagulants
▪ GCS didnot return to 15 within 2-3 hours
▪ Vomiting >2 episodes
▪ Skull fractures: open, depressed or basilar
▪ Focal neurological deficits
◦ Relative:
 ▪ Amnesia before impact for >30 minutes.
▪ High energy mechanism
▪ Loss of consciousness for >5 minutes at any point after injury.
◦ Moderate injury (GCS 9-12): All patient admitted atleast for 24 hours for observation
and their head CT should be obtained.
◦ Severe injury (GCS <8): Requires urgent specialist care.
• Medical management:
◦ Hyperventilation in case of acute herniation to keep pCO2 <30
◦ Mannitol in acute neurological worsening (e.g pt. Under observation develops new
FNDs) to quickly decrease ICP. It is not effective in hypotensive patients and in fact
worsening brain injury due to ischemia thus IMP. To r/o shock in patients.
◦ Hypertonic saline can also decrease ICP as effectively as mannitol and used as
alternative.
◦ Barbiturates decrease ICP but not to be used in hypovolemia or low BP.
◦ Anticonvulsants for post traumatic seizures. Prophylaxis not recommended because no
evidence of any long term benefit, in fact anticonvulsants may inhibit brain recovery.
◦ Prevent pyrexia onset as it increases brain oxygen demand. Managed by inducing
therapeutic hypothermia.
◦ Nutrition: Enteral nutrition. Prokinetics (metoclopromide, erythromycin) to promote
absorption
• Surgical management
◦ Depressed skull fracture: Surgical elevation when degree of fracture depression is
greater than adjacent skull thickness or when the fracture is open or contaminated.
◦ Intracranial mass: Require urgent neurosurgical care. Procedure of choice: Craniotomy.
◦ Penetrating injury: CT is IMP. Esp. When bullet trajectory passes through or near skull
base or major dural venous sinus.
Orbito-facial or pterional region injury produces aneurysms and AV fistulas that is
identifiable on CT angiography and requires surgical or endovascular management.
• Brain death:
◦ Requires criteria of:
▪ GCS <3
▪ Non reactive pupils
▪ Absent brainstem reflex
▪ No spontaneous ventilatory effort on formal apnea testing
▪ Absence of confounding factors like hypothermia, drugs like barbiturate and alcohol.
◦ Supportive investigations:
▪ EEG: No activity at high gain
▪ Cranial blood flow study (isotope, doppler, xenon CBF studies): No cranial blood
flow.
▪ Cerebral angiography.
◦ Paediatric patients can recover from severe brain injuries and diagnosis of brain death in
these always done after multiple placed serial exams.

Spinal Trauma
General points
• Spinal cord injuries can occur with blunt or penetrative force. Blunt injuries damage by
direct spine impingement or by accumulation of blood and edema impinging on spinal cord
whereas penetrative injuries can directly damage cord or cause injury by ischemia or spinal
fracture. Cervical spine is most prone to injury as it most mobile and even in that C5-C6 is
most mobile among all so it is most prone to inury.
 • Spinal trauma is associated with concomitant head trauma and lower vertebral trauma.
• Neurogenic shock: It is the loss of vasomotor and sympathetic innervation to the heart due
to injury to thoracic and cervical spinal cord levels (T6 and above), causing unopposed
vagal/parasympathetic effect which results in vasodilation of blood vessels and pooling of
blood causing hypotension, its effect on heart results in either bradycardia or inability of
tachycardic response. IMP. To r/o hemorrhagic shock as that can also cause hypotension.
Vasopressor may be required with fluid therapy to maintain MAP & atropine for
bradycardia.
• Spinal shock: It is the flaccidity (loss of muscle tone) and loss of reflexes occurring
immediately after spinal cord injury period of time after which there is spasticity,Absence of
bulbocavernous reflex is diagnostic. It lasts 24 hours after injury then resolves with 1st sign
of resolution being return of bulbocavernous reflex.
• Main concern is respiratory failure due to hypoventilation occurring from paralysis of
intercostal muscle.
• Pain to other body sites may also be absent masking any serious injuries.
• Patterns of spinal cord injury:
◦ Central cord syndrome: Presents with disproportionate upper limb motor deficits than
lower limb & varying sensory loss. This occurs in context of hyperextension injury
sustained from forward fall & facial impact in established cervical stenosis with or
without any presence of cervical fracture/dislocation.
◦ Anterior spinal syndrome: presents as Bilateral loss of pain and temperature sensation
with spastic paraplegia (lesion below cervical level) or quadriplegia (lesion at cervical
cord level). Pressure, vibration & propioception is intact due to preserved dorsal
columns. Such patterns mostly seen with anterior spinal artery insufficiency.
◦ Brown-sequard syndrome: Occurs with penetrative injury causing hemisection of spinal
cord. It presents with ipsilateral spastic weakness with loss of pressure, position &
vibration sense, contralateral pain and temperature sensation loss 1-2 levels below lesion
and flaccid weakness at same level of lesion.
Clearing spine injury
• To be done after stabilising patients. Until then C spine is protected using cervical collar or
voluntary restriction of movement, Spinal board to be used only for transportation,
otherwise to be avoided because it causes pressure ulcers.
• Involves clinical and radiographic criteria.
◦ NEXUS criteria: Presence of any of these low risk criteria:
▪ No posterior midline spinal tenderness: from nuchal rigidity upto 1st thoracic spine.
▪ No e/o focal neurological deficits
▪ No e/o intoxication: No h/o observing intake or physical signs of intoxication.
▪ No distracting injury: Injury so painful it might distract from potential spine injury
like long bone fractures, large laceration, visceral injury, large burns or any other
injury causing acute functional impairment etc.
▪ If all above criteria are present then no need for a radiography and patient can be
cleared. If any present then a radiograph is taken.
◦ Canadian C spine rule: It is applicable in patients who are alert and with GCS =15. In
this presence of any high risk & absence of any low risk factors indicate need for
radiography, presence of low risk factors is followed up with physical examination
which determines need for radiography.
▪ High risk criteria:
• Age >65
• Dangerous mechanism of injury: fall from a height >1m/5 stairs, an axial load to
the head, a motor vehicle collision either at high speed or with rollover or any
ejection, motorized vehicle collision or bicycle collision.
• Paresthesia in extremities
 ▪ Low risk criteria: Simple rear end motor vehicle collision, Sitting position in
emergency department, ambulatory at any time, delayed onset of neck pain, No
midline cervical spinal tenderness.
▪ If low risk factors are present then follow-up cervical spine examination by eliciting
neck rotation is performed. If neck rotation to 45 degrees can be performed then no
need for neck radiography otherwise if it cannot be performed then we need cervical
spine imaging to confirm injury.
• Imaging is done by either MDCT or X-ray lateral view of spine. If no injuries detected on all
7 vertebrae by these then X-ray AP view and swimmer’s view are taken. Films are assessed
for:
◦ Bony deformities/fractures of vertebral body/processes.
◦ Loss of alignment of posterior aspect of vertebral body (anterior extent of vertebral
canal).
◦ Increased distance b/w spinal process at one level.
◦ Narrowing of vertebral canal.
◦ Increased pre-vertebral soft tissue space.
◦ Instability:
▪ 3.5mm of sagittal translation
▪ Sagittal angulation of >11 degrees.
• If no injuries present in all types of radiographs then flexion-extension MRI images taken to
evaluate for ligamentous injuries, it is also needed if patient presents with severe paraspinal
muscle spasm.
Specific injuries and management
• Spinal cord columns: Spinal column is divided into 3 columns, anterior, middle and
posterior. Anterior column is anterior 2/3rds of vertebral body with anterior longitudinal
ligament, middle column is posterior 1/3rd of vertebral body with posterior longitudinal
ligament and posterior column is all structures posterior to posterior longitudinal ligament.
• Burst fractures of spine occurs when there is involvement of anterior and middle columns of
spine and compression fracture occurs when there is involvement of only anterior column of
spine. Burst fractures occurs with axial loading and it is a/w other fractures forming
characteristic pattern involving calcaneal fracture, tibial plateau, and proximal femur
fracture.
• Cervical spine fracture: Can happen with axial loading, flexion, extension, distraction and
lateral bending. In children it is rare. Specific subtypes are atlantoaxial dislocation, atlas
fracture, C1 rotatory subluxation and axis (C2) fracture.
◦ Atlantoaxial dislocation: From severe Traumatic flexion and distraction. Most die early
from brainstem compression and apnea other they have profound neurological
impairments (ventilator dependence, quadriplagia/hemiplegia). This fracture is seen in
shaken baby syndrome.
◦ Occipital condyle fracture: Associated with head injury, treated with hard collar for 8
weeks.
◦ C1 fracture: less then half is asso. C2 fracture, MC type is Burst (Jefferson) fracture
which happens MC by axial loading from falling on one’s head or something heavy
falling on head, confirmed on radiographs by presence of instability suggested by
disruption of anterior and posterior rings with lateral displacement of lateral masses, if
only one side ring and lateral mass is involved then it is stable. Tt: if stable transeverse
ligament: Non operative with halo or collar brace. If unstable transeverse ligament:
Surgery or traction.
◦ C1 rotatory subluxation: Mostly seen in kids, can happen spontaneously with
major/minor trauma, upper respiratory tract infection or with rheumatoid arthritis.
Patient has persistent rotation of neck (torticollis). Odontoid is not equidistant from
 lateral masses in C1. Patient head not to be forced to normal position instead restrict all
motion and consult specialist.
◦ C2 axis fracture: less commonly involved than C1. Main subtypes are odontoid fracture
and posterior element fracture.
▪ Odontoid fracture: is of three types,
• Type 1 is fracture of tip of the odontoid and its rare Tt: Hard collar.
• Type 2 is fracture of base and is more common. In kids <6 y/o X-ray may falsely
appear as this fracture due to prominent epiphysis at this age. Tt: halo vest or
surgery.
• Type 3 occurs in base of dems and extends obliquely in body of the axis. Tt: Halo
vest.
▪ Posterior element fracture: Also called the hangman’s fracture, involves the fracture
of posterior element of C2, the pars interarticularis, it is usually caused by extension
type injury. Rigid collar is a must, needs specialist care, most cases treated
operatively and requires posterior stabilization or with Halo vest.
◦ Other cervical fractures: C5 most prone to fracture, C5 on C6 most prone location for
subluxation. Tt: If mild loss of height then hard collar. If Involvement of multiple
columns or propulsion of fragments into vertebral canals: Surgical stabilization.
• Thoraco-lumbar injuries:
◦ Thoracic: Most common types are wedge compression fracture, burst fracture, chance
fractures & fracture-dislocations. If a/w sternal fracture there is significant risk of aortic
rupture, if a/w multiple posterior rib fractures & dislocations above and below spinal
injury then significant vascular injury may be present.
▪ Anterior wedge compression fracture: Mainly caused by flexion with axial loading.
Mostly stable due to rib cage. Treated with rigid brace.
▪ Burst fracture: From vertical axial loading. Tt: Internal fixation
▪ Chance fracture: Seen in motor vehicle accident where driver & shotgun restrained
by only seatbelt. Tt: Internal fixation
▪ Fracture-Dislocations: Rare, happens in injuries causing extreme flexion or severe
blunt trauma to spine, disrupting posterior elements. Because thoracic canal is
narrow in relation to spinal cord, hence fracture-subluxations commonly produce
complete neurologic deficit. Tt: Internal fixation
◦ Thoraco-Lumbar (T1-L11): Occurs with falls and in restrained drivers causing severe
hyperflexion. Very vulnerable to rotation and can worsen with logrolling. Can lead to
bladder & bowel dysfunction & decreased sensation & strength in lower extremities.
Osteoporotic wedge compression fracture is common in this level & it is managed
nonoperatively if there is no significant loss of height (>25%) in symptomatic case
(i.epain limits patient recovery) it is managed with percutaneous bone cement
augmentation called vertebroplasty or kyphoplasty.
Burst fracture is a type of comminuted fracture at this level leading to retropulsion of
fragments in spinal canal, needs surgical corpectomy as a management
If only anterior column is injured of thoracolumbar levels then thoracolumbar orthosis is
used for management, if both anterior & posterior column are involved then surgical
stabilization is done.
General Management
• Restrict spinal motion below suspected injury site till fracture excluded (except in cases of
penetrative injuries when there is no demonstratable benefit). Done by placing them on rigid
surface supine and wearing cervical collar. No attempt should be done to reduce obvious
spinal deformities. Children with torticollis and elderly with kyphosis from degenerative
spine diseases should receive spinal restriction at recumbent position of comfort. Attempts
to align spine to restrict its motion on backboard should be stopped if it causes pain.
Supplementation with bolts and straps on spine board is more effective than rigid cervical
 collar. Logroll is performed to remove the spine board.
Raising the head of the bed helps in airway in such patients.
• Neurogenic shock: Suspected when patient is hypotensive and no sites of hemorrhage are
found and signs of bradycardia instead of tachycardia. Vasopressors indicated like
phenylephrine, norepinephrine, dopamine. Fluid overload in these cases cause pulmonary
edema. Urinary catheterization is important to prevent bladder distension.
• Type of surgery depends on type of injury, in general spinal decompression gives best result
if performed within 24 hours of injury. Cervical fracture dislocation may benefit from
applying traction. Spinal instability requires surgery, whereas if stable enought they can be
managed with immobilization only with hard collar or brace and follow-up upright X-rays
until bone healing can occur.
Complications
• Pain & spasticity: Once reflex activity returns following injury, then spasticity may occur
and be problematic. Tt with intrathecal baclofen in resistant cases.
• Autonomic dysreflexia: Paradoxial hypertension, hypohydrosis (above injury level),
flushing, headache & bradycardia in response to noxious visceral or other stimuli, most
commonly triggered by bladder distention or fecal impaction.
• Post traumatic syringomyelia: Causes late (>3months) neurological deterioration, occurring
in 3-5% spinal injury cases, Increase in pain and/or spasticity, Ascending loss of sensation &
Deep tendon reflexes warrant early MRI, expanding central spinal cavities require
neurosurgery.
• DVT & PE: Requires low molecular weight heparin.
• Disuse osteoporosis, heterotopic calcification & contractures.

Neck Injury

General Points
• Highest mortality than trauma to any other region.
• Injuries from any mechanism leads to haematoma and oedema deep in neck tissue leading to
displacement and obstruction of airway, also larynx and trachea may be disrupted (MCC) or
there may be severe haemorrhage in tracheobronchial tree. Initially the obstruction may be
only partial and the patient may be able to maintain patency and ventilation which presents
as noisy breathing, but then airway would get progressively compromised resulting in
complete obstruction which appears as absence of breath sounds, hence for these reasons it
is necessary to establish emergent airway.
Attempted airway might worsen the compromise hence requiring a backup plan in form of
cricothyroidotomy or tracheotomy.
• Penetrative injuries may cause vascular and aerodigestive tract injuries with the latter
contaminating the surrounding areas.
• Blunt trauma causes compression with subsequent fracture of larynx and trachea, although
rare it can also damage pharyngeal and oesophageal tract causing tissue devitalization and
contamination.
◦ May also injury carotid and vertebral arteries so called Blunt cerberovascular injuries
(BCVI) commonly in situations of seat belt injuries and severe flexion & extension
injuries. Injuries may range from intimal tear with or without thrombosis (Grade 1) to
full thickness rupture with pseudoaneurysm formation (Grade 3) & transection (Grade
5).
• Laryngeal trauma: Presents with hoarseness, subcutaneous emphysema & palpable fracture.
Management
• Hemodynamically unstable patients, patients with hards signs of vascular injury or
aerodigestive injury i.e expanding or pulsatile hematoma, airway compromise, subcutaneous
emhysema , air bubble coming through the wound, neurologic deficit & hematemesis should
be quickly taken for emergent surgical exploration & repair.
• Stable patients can be further evaluated clinically and through imaging to determine
conservative or surgical management.
• Penetrating injury can be classified into 3 zones based location of injuries, which have
varying degrees of seriousness of injuries:
◦ Zone 1 is located b/w thoracic inlet and cricoid cartilage containing trachea, esophagus
and large vascular structures.
◦ Zone 2 is located b/w cricoid cartilage and angle of mandible containing aerodigestive
tract, jugular vein, vertebral and carotid artery. It is the zone most easily accessible
through surgery. Injuries at this zone is suggested by physical exam finding of defect in
platysma which if present, traditionally referred for surgical exploration, however
nowdays only those with hard signs of injury are referred for surgery.
◦ Zone 3 is located b/w the part of neck in between angle of mandible to base of skull, it
contains mainly blood vessels. It is the zone the hardest to access through surgery.

• Penetrating injuries are best evaluated using CT angiography.

• Blunt cerebrovascular injury should be suspected in all cases with high risk features of:
◦ Signs and symptoms:
▪ Expanding neck haematoma
▪ Arterial blood loss from neck, nose or mouth
▪ Focal neurologic deficits
▪ Cervical bruit (patient <50 year old)
▪ Stroke on CT or MRI
 ▪ Neurologic deficit unexplained by CT finding
◦ high risk factors:
▪ Severe midface fractures: lefort 2 or 3
▪ Basilar skull fracture involving carotid canal
▪ Diffuse axonal injury and GCS score <6
▪ Significant cervical spine fracture or ligamentous neck injury
▪ Significant soft tissue injury to anterior neck (i.e seat belt mark)
▪ Near hanging with anoxia.
• These patients should be screened for BCVIs with MDCT if they have any of the following
features:
◦ Any injury above clavicle regardless of mechanism
◦ Neurological examination unexplained by imaging
◦ Horner syndrome.
• Blunt aerodigestive injury is very rare, hence no such screening criteria.
• BCVI treatment: Anticoagulation and antiplatelet, endovascular stenting in Pseudoaneurysm
and dissection with 70% flow limitation. Anticoagulation and anti-platelet therapy to be
initiated as soon as safely possible to prevent interfering with management of bleeding from
other injuries, even delayed initiation over days to weeks can still be beneficial. The patient
is followed up with MDCTA again over 7-10 days to confirm progression or resolution with
subsequent discontinuation of therapy. Persistent injuries may require 3 months of therapy
with outpatient MDCTA.
Musculoskeletal injury

General Points
• These injuries are infrequently life threatening but distract from other life threatening
injuries.
• Major injuries can denotes presence of significant force or pathology, for e.g :
◦ Involvement of limbs above and below diaphragm suggests injury to torso or abdomen.
◦ Unstable pelvic fracture and open femur fracture can be a/w brisk bleeding.
◦ Severe crush injuries a/w renal failure from rhabdomyloysis induced myoglobinuria. Or
cause compartment syndrome from swelling into myofascial compartment
◦ Long bone fracture a/w fat embolism
• Musculoskeletal injuries should not be postponed for evaluation later and should be included
in primary survey.
• If reduction is required then it must be done ASAP as with increasing time it becomes
difficult due to tissue edema and muscle spasm.
Primary survey
• Potential life threatening conditions involved are major arterial hemorrhage, B/L femoral
fracture, crush syndrome & pelvic disruption (mentioned above).
• Arteries get invovled if there has been deep soft tissue lacerations.
 • Best way for hemorrhage control is direct pressure
• Long bone fracture cause significant haemorrhage esp. Femoral fracture which bleed heavy
into thighs.
• To control bleeding from long bones best method is splinting which reduces limb motion
and provides a tamponade effect on muscles and fascia.
• For open fractures sterile pressure dressing to control haemorrhage. Any exposed bone is
pushed back into wound as open wounds require surgical debridement, gross contamination
and particulate matter is removed and weight based antibiotic dosage given.
• Fluid supplementation as important supplement.
• Resuscitation is important than splint application.
• Joint dislocation may warrant an attempt at reduction, if closed reduction successfully
relocates joint then immobilize it at that location with splint, pillows or plaster to maintain
reduction. If reduction unsuccessful then immobilize joint in position in which it was found.
Apply splints ASAP as it controls pain and hemorrhage.
• X-ray may be done if long bone fracture is a suspected cause in a current shock case.
Management of life threatening conditions in Primary survey

Major arterial hemorrhage and traumatic amputation

• Can occur with penetration into artery, blunt injuries causing fracture near a vessel or joint
dislocation near and artery.
• Appears as significant bleeding into soft tissue or exsanguination from an open wound.
• Important physical signs of arterial hemorrhage is absent previously palpable pulse,
diminished pulse, change in pulse quality, decreased ankle brachial index. Cold pale
pulseless extremity suggests significant interruption in arteiral supply whereas a rapidly
expanding hematoma suggests severe vascular injury.
• Management:
1. Manual pressure to wound
2. Pressure dressing on wound (gauze + circumferetial elastic badndaging)
3. Application of manual pressure in artery proximal to injury (if bleed not stop by now)
4. Application of manual tourniquet like windlass device or pneumatic tourniquet directly
to skin (most severe measure if nothing else controls bleed)
▪ Tourniquet should be tied appropriately to block both arterial and venous drainage
else occluding only venous drainage can result in hemorrhage, swollen cyanotic
extremities
▪ proper documentation of time when tourniquet worn is important.
▪ Tourniquet may be deflated if time to operative intervention is taking longer than 1
hr in stable patients.
▪ Risk of tourniquet use increases with time, and have to balance life v/s limb risk.
5. In stable patients arteriorgraphy and other diagnostic investigations can be performed, in
unstable patients or those with clear vascular injuries they should be taken emergently to
surgery.
▪ Vascular clamps through open wound only for superficial vessel haemorrhage
▪ If haemorrhage a/w fracture realignment and splinting of fracture while keeping
pressure on the open wound.
▪ Haemorrhage a/w joint dislocations should be managed by quickly reducing the
dislocation.
6. Amputees require tourniquet application and urgent surgery consultation. Certain
mangled extremitites with prolonged ischemia, nerve injury and muscle damage may
require surgical amputation, it can also be beneficial in patients having hemodynamic
abnormalities resulting from the injured extremities.
7. Replantation is considered in conjunction with other injuries i.e patient with multiple
injuries needing intense resuscitation or emergency surgery is not candidate for
 replantation. Replantation is usually done for patients with isolated single limb or part
thereof.
▪ Amputated part must be thoroughly washed stored carefully in saline or ringer
lactate soaked moist sterile gauze, then wrap it again with moistened sterile
cloth or towel, place it in a plastic bag and that bag is placed inside a plastic bag
with ice or any container with ice. Ice should not directly touch the part or else it
would cause injury.
8. Absolute indications of amputating limbs is:
◦ Severe crush injuries.
◦ Mangled stump.
◦ Distal tissue not amenable to repair.
◦ Missing extremity.
◦ Extremity with warm ischaemia time >6hrs. Warm ischaemia time (WIT): The time
a tissue/organ/part has remained at a body temperature from the time where its
blood supply has been cut-off but before it is cooled or reconnected to a blood
supply.
▪ A MESS (mangled extremity severity score) score calculated using vascular
status, age of patient, duration of ischemia and absorbed energy if is >7 may
suggest amputation of limb but is not always the case hence used with caution.

B/L femur fracture

• Occurs in setting of application of significant force, and should be alerted for associated
injuries.
• They are significantly more likely to develop severe hemorrhage pulmonary complications,
multiple organ failure and death.
• Requires early transfer to a trauma center.

Crush Syndrome
• A state of untreated injured muscle causing acute renal failure and shock.
• Often in setting of severe compression of injury of a significant muscle mass like calf or
thigh which leads to muscle injury ischaemia and eventually death resulting in myoglobin
release.
• Myoglobin tests positive as haemoglobin in urine dipstick test, it can be confirmed by nor
RBCs or RBC casts on urine microscopy, or by myoglobin assay, if not available an amber
colored urine with creatinine kinase levels >10,000 IU/L is s/o rhabdomyolysis.
• Further complications can be, metabolic acidosis, hyperkalemia, hypocalcemia,
hyperphosphatemia and DIC.
• Tt: Early aggressive Fluid resuscitation is critical to protect kidneys & prevent renal failure.
Once Myoglobin induced renal failure sets in it can be managed with alkalinization of urine
by IV bicarbonate and osmotic diuresis.
Secondary survey
• Essentially ivolves 3 main goals, to assess life threatening injuries, limb threatening injuries
and to find out any missed musculoskeletal injuries.
• Visual inspection of whole body assessing color, perfusion, wounds and deformities.
◦ Pale white extremity is s/o lack of arterial inflow
◦ Swelling in major muscle group is s/o crush injuries with impending compartment
syndrome
◦ Swelling or ecchymosis in and around joint s/o musculoskeletal injury
◦ Extremity deformities denote serious joint injuries:
▪ Shoulder joint dislocation: Anterior=Squared off deformity, Posterior= Locked into
Internal rotational
 ▪ Posterior elbow disloction: Olecranon prominence
▪ Hip dislocation: Anterior= Extended abducted, externally rotated, Posterior= Flexed,
Adducted, internally rotated
▪ Knee anteriorposterior dislocation: loss of normal contour, extended
▪ Ankle lateral dislocation: Externally rotated, prominent medial malleolus
▪ Subtalar lateral dislocation: Laterally displaced os calcis
◦ Log roll patient for any open wounds in dorsal body. Open wound associated with
fracture is considered open fracture till proven otherwise.
◦ Spontaneous motor extremity function should be assessed. In unconscious patients it is
the only sign of impaired function.
• Palpation for tenderness, deformitites and abnormal bone motion. Tenderness may denote
fracture, although pain, tenderness & swelling a/w deformities or abnormal motion through
bone is more s/o fractures. Do not attempt to elicit creptius or demonstrate abnormal motion.
Joint stability can only be determined by clinical examination abnormal motion indicates
ligamentous or tendinous injury further suggested by presence of their swelling on
palpation, confirmed by cautious stressing of ligament and tendon, excessive pain may mask
their injuries due to guarding of the joint by muscular contraction or spasm.
• Circulatory assessment by palpating distal pulses and assessing capillary refill, if
hypotension limits assessment, doppler probe can be used to assess circulation, loss of
sensation in stocking or glove distribution is earliest sign of vascular impairment. In patients
with normal BP arterial injury suggested by pulse discrepancies, coolness, pallor,
paresthesias & motor function abnormalities. Open wounds and fractures closest to arteries
also suggest possible arterial injury. Expanding hematoma or pulsatile hemorrhage also
suggests arterial injury. Ankle brachial index <0.9 also s/o of arterial injury.
• Do X-ray in patients with tenderness and joint deformity, patient haemodynamically stable
and with joint effusion, joint tenderness and joint deformity, the only reason to forego X-ray
in these patients is if there is impending vascular compromise or skin breakdown (which is
commonly seen in ankle fracture-dislocations)

Limb threatening injuries

Injuries potentially considered are open fracture, ischemic vascular injuries, compartment
syndrome, neurologic injury secondary to fracture or dislocation.
Open fractures
• Defined as Fracture with an associated open wound in direct contact with surrounding
enviornment. Said to be when hematoma a/w fracture is exposed by a breach in epithelial
surface which is usually skin but can be bowels or vagina.
• Open fractures are diagnosed when open wound on same limb segment with the associated
fracture.
• If Open wound at or near a joint then suspect open Joint injury, it can be confirmed with
presence of intrarticular gas on CT or insertion of saline or dye in the joint cavity and
observing extravasation of it through the open wound to see if it communicates with the
joint.
• Fracture a/w high velocity gunshot wound and shotguns are treated as open wounds.
• Tt: All open fracture patients immediately treated with IV antibiotic preferably 1 st gen
cephalosporin like cephazolin, max delay upto 3hrs no effect thereafter. Remove gross
contaminates and particulates from wound and cover with moist sterile dressing and
immobilized. Patients is stabilized and only thereafter undergo surgical debridement &
fracture stabilization.
Intraarticular gunshot
Bullets or gragments lodged inside joints can cause plumbism & systemic lead toxicity, breakdown
of articular cartilage and development of early arthritis from third body wear requiring urgent
exploration and removal of the bullet done by open arthrotomy or with arthroscopic assitance.
Bullets traversing joints without retention are not a/w increased infection rate and do not require
formal irrigation and debridement.
Vascular injury
• Should be suspect in cases of vascular insufficiency.
• Is mainly of 5 types, 1) intimal injruy, 2) complete wall defects with pseudoaneurysms or
hemorrhage, 3) complete transection with hemorrhage or occlusion4) AV fistulas and 5)
spasm. Blunt trauma causes mainly intimal injury whereas penetrating trauma causes latter
grade 2-5 injuries.
• Initial vascular insufficiency may not be apparent due to supply from collaterals, non
occlusive vascular injuries like intimal tear can cause coolness & prolonged capillary refill
in distal extremities as well as diminished peripheral pulses and abnormal ankle brachial
index. Complete vascular disruption presents as cold, pale & pulselessness. Paresthesias,
paralysis, rapidly expanding hematoma, palpable thrill or audible bruit, relative loss of
doppler signals & obvious massive bleeding are also signs of vascular injury.
• Tt: Is emergent, takes priority above all, manual or operative revascularization can be
performed. If there is associated fracture deformity, correct it by gently pulling limb out to
the length, realigning the fracture and splinting the injured extremity such manoeuvrers
restore blood flow caused by kinked arteries due to shortening and deformity at fracture site.
If such reduction not possible the limb should be splinted and urgent surgical consult should
be obtained, although that itself may cause vascular compromise ,hence check neurovascular
status before and after splinting, deterioration of which is suggested by loss of or change in
distal pulses or excessive pain after splinting, if any of these present promptly release all
splints, casts or any other circumferential dressings and then reassess vascular supply.
Compartment syndrome
• Happens with increased pressure in musculofascial compartment which happens with
increase in compartment content (e.g bleeding into compartment or swelling after
revascularization) or a decrease in compartment size (e.g with a constrictive dressing).
Compartment syndrome happens anywhere there is muscle enclosed within a closed fascial
space, even enclosure by skin.
• Certain injuries are high risk to develop compartment syndrome:
◦ Tibia and forearm injuries
 ◦ Crush injuries
◦ Burns
◦ Ischemia reperfusion causing increased capillary permeability
◦ Excessive excercise
◦ Injuries immobilized to tight dressing or cast
◦ Localized, prolonged external pressure to an extremity
• Absence of pulse, diminished capillary refill times and weakness or paresis of involved
muscle or limb are seldom present or be a late finding hence unreliable features to diagnose.
Dx made clinically if suggestive features of pain out of proportion to received
injury/stimulus, pain on passive stretch of affected muscle & tense swelling of compartment,
it can be confirmed with measurement of compartment pressures, with pressures >30mmhg
suggesting diminished capillary flow.
• Tt: Prompt release of all constrictive dressings, casts and splints applied over affected
extremities and immediately obtain surgical consult. The only treatment for this syndrome is
surgical fasciotomy any delays might result in myoglobinuria and renal failure. Fasciotomy
has it sown complications,it converts a fracture into an open fracture prone to infections and
delaying union of bone, it also promotes scarring, muscle weakness and causes prolonged
pain.
Neurologic injury
• Thorough neurologic examination for each peripheral nerve must be performed, for each
nerve voluntary motor function and sensation must be assessed. Progression of neurological
finding is indicative of continued nerve injury.
• Tt: reduction and splinting of fracture deformity.
Other injuries
• Crush injury may be subtle and recognized based on devascularization and necrosis of
muscle
• Internal degloving injuries: Soft tissue avulsion can shear skin from deep fascia allowing
significant accumulation of blood in resulting cavity ( Morel-lavalle lesion) alternatively
skin may be sheared from blood supply and undergo necrosis over few days such areas have
overlying abrasions and bruised skin.
Missed Injuries
Injuries Missed/Associated Injuries
• Clavicular fracture • Major thoracic injury esp. Pulmonary
• Scapular fracture contusion and rib fracture
• Fracture and/or dislocation of shoulder • Scapulothoracic dislocation
• Fracture/dislocation of elbow • Brachial artery injury
• Median, ulnar or radial nerve injury
• Femur fracture • Femoral neck fracture
• Ligamentous injury of knee
• Posterior hip dislocation
• Posterior knee dislocation • Posterior hip dislocation
• Femoral fracture
• Knee dislocation • Popliteal artery and nerve injuries
• Displaced tibial plateau
• Calcaneal fracture • Spine injury or fracture: Burst fracture
• Fracture dislocation of talus and
calcanuem
• Tibial plateau fracture
• Open fracture • 70% incidence of associated
nonskeletal injury
Specific fracture management
• Femoral shaft fracture: Intramedulllary nailing
• Tibial shaft fracture: If stable (A-type): Casting, full leg cast. If instability: Intramedullary
nailing, however it has a side effect of anterior knee pain. In instability cases where fracture
is close to tibial metaphysis, nailing is not preferred instead plating is done, because
malunion is common after nailing in fractures of proximal tibial shaft.
• Humeral shaft fracture: treated nonoperatively with brace and collar. In cases of multiple
injuries, head injuries, it is treated operativey with internal fixation using nails and plating.
• Radius and ulna fractures: Treated with i\open reduction and plate fixation to achieve
precise anatomical restoration.
 • Metaphyseal fractures: These are of 3 types A,B & C. A type is extra articular, B type is
partial articular and C type is intrarticular. There are main problems with metaphyseal
fractures. 1st is joint stiffening resulting from fractures so close to joint and 2nd is that there
are 2 very different types of bone around the fracture location, one is stiff (diaphysis ) &
easier to achieve internal fixation in and another is spongy (Metaphysis) difficult to achieve
the same, the widely varied types of bone lead to imbalance in internal fixation and lead to
failure of internal fixation.
• Distal radial fractures: Most of them are type A fractures. Colles fracture with dorsal and
radial angulation can be treated with manipulation and casting and intrafocal wiring only if
instability. In volar displacement of radius, stability is difficult so plating is done.
• Ankle fracture: If stable then only symptomatic treatment, if instability then open reduction
and internal fixation especially in young patients. No clear benefit in surgery v/s
conservative in elderly.
• Pelvic ring disruption: Instability suggested by translation in vertical plane of >1cm through
either a sacral fracture or sacroilliac joint. Fracture of transverse process of L5 should also
raise suspicion for pelvic instability secondary to disruption of illiolumbar ligament.
Osteoporotic fractures
• Elderly have difficulty tolerating weight even partial, hence fixation must be able to tolerate
full weight bearing.
• Reduction failure common due to hold of screws being poor and backing out of screws.
Locking plates help overcome the problem.
• Intrarticular fractures: Post traumatic arthritis a low concern, joint stability more concern
than congruity, in stable joints nothing done, reconstruction via bone grafting may be
required.
• Proximal femoral fracture: Of 2 types intracapsular and extracapsular. Intracapsular fracture
compromise the blood supply of femoral head and are thus treated differently.
◦ Extracapsular fractures: Treated with indirect reduction using traction table followed by
fixation using dynamic hip screw (DHS) placed using image intensifier. This implant
allows movement of fragments closer together when patient walks allowing ambulation.
◦ Intracapsular fractures: Most are elderly and osteoporotic. In elderly early mobilization
is goal to promote independence. If fracture is displaced then blood supply has been
compromised and there is no point to reduce the fracture as the femoral head is dead
(avascular necrosis), hence the treatment of choice is to simply replace the compromised
femoral head with and artificial head ( a hemi-arthroplasty), this cannot be done in
younger patients because the femoral head might still be viable esp. If undiscplaced
fracture, in which case we attempt to reduce and fix fracture, holding with screws placed
under image intensifier tool or to perform a total hip replacement.
• Calcaneal fracture: Largest and most frequently fractured hind foot bone, a/w spine
fractures. Plain radiographs inadequate to assess degree of damage and need CT for proper
assessment. Tt can be manual reduction and fixation but a effective reduction is difficult to
achieve and hence requires surgery.
• Talus fracture: has weak bloody supply due to absence of any muscular or tendinous
attachment. Talar neck fracture is the most common fracture type and usually high energy, a
significant complication is avascular necrosis of talus. Goal is anatomical reduction and
stable fixation. Viability of talus depends on intact blood supply which can be determined by
X-ray finding of Hawkin’s sign which is subchondral lucency of talar dome signifying bony
resorption, absence of this sign suggests osteonecrosis of talus showing only subchondral
sclerosis and suggesting disrupted blood supply.
 • Achilles tendon rupture: Patients present with sensation of getting kicked in the ankle from
behind, sometimes palpable gap may be present behind heel, Simond’s sign is positive
(squeezing calf muscle do not produce plantarflexion which it ought to if achilles tendon
was intact), differentials are intrasubstance tear in gastrocnemius muscle in which the
simmond’s test is negative (plantarflesion with calf squeezing although painful), Dx of
achilles tendon rupture made with USG, if gap b/w torn ends is small patient treated with
serial plasters, in patients with wider gap, (>5mm), a percutaneous repair can be done.
• Scaphoid fracture: Scaphoid waist fractures are usually common, this happens with fall on
outstretched hands with hands in radial deviation and dorsiflexion, waist fracture displaces
proximal and distal part of scaphoid and since the proximal pole receives blood supply
retrogradely coming through the distal pole it is prone to avascular necrosis. O/E there is
tenderness at anatomical snuff box, X-ray may not show a fracture line for upto 10 days,
hence even at equivocal examination patient’s hand immobilized in wrist and thumb cast, to
reduce risk of non union and avascular necrosis, examination is repeated again 10-14 days
later, if now the fracture line is seen, cast is maintained further for 6 weeks, if X-ray again
equivocal and clinical suspicion remain MRI is done. Surgery indicated in Unstable
fractures in which there is >1mm displacement b/w parts or any angulation.
• Lunate dislocation: Presents clinically as swollen wrist which clinically means dissociation
of carpus, Dx made on carpal radiograph which is difficult to interpret, lateral view
demonstrates the ‘Spilled Teacup sign’ with volar tilt of lunate. Acute injuries can be
initially treated with closed reduction and casting. Irreducible and acute injuries require,
open reduction and stabilization with K wires.
Dislocations
• All dislocated joints posit possible neurovascular injury and damage to articular surface and
are considered orthopaedic emergency, prolonged dislocations cause, cartilage, death,
posttraumatic arthritis, ankylosis and avascular necrosis.
• Evaluation:
◦ Joint’s range of motion very limited
◦ Muscles in the region have high tone
◦ Pathognomic positions
▪ Hip joint: most are dislocated posteriorly so thigh will be internally rotated, flexed
and limb shortened.
 ▪ Shoulder: Classically anteriorly dislocated so arm is externally rotated and adducted.
In thin patients loss of normal contour of deltoid
◦ Associated fractures, 70% of hip dislocations a/w acetabular fractures, humeral head
dislocation a/w glenoid rim fracture.
• Complications:
◦ Hip dislocations: Sciatic nerve injury, avascular necrosis and cartilage death
◦ Knee dislocations: popliteal artery injury.
• Tt: Manual reduction ASAP, except if in knee there is presence of “ dimple sign” which is
furrowing at anteromedial aspect of femur, suggesting femoral condyle protrusion through
the soft tissue denoting that the dislocation is irreducible and multiple attempts should not be
made unless risking skin necrosis, surgical reduction is indicated in such cases.

Thermal injury
General points
• Main goals are to maintain airway, hemodynamic status, controlling temperature, managing
environment, management of associated mechanical injuries and other complications
secondary to thermal injury mechanism.
• Consequence of burn injury is directly linked to extent of inflammatory response to burn:
The Larger & deeper the burn the worse the inflammatory response.
Primary survey
• Decontaminate by removing any clothing contaminated by chemicals, brush off any dry
chemicals, decontaminate the area by rinsing with copious amount of warm saline irrigation,
or rinsing in warm shower. After contamination cover patient with warm clean dry linen.
• All rings, watches, jewellery, and belts should be removed because they retain heat and can
produce a tourniquet-like effect.
• Room temperature water to be copiously poured over wound within 3hrs of injury to
decrease depth of wound and improve healing.
• Airway: Obstructs from direct injury or edema secondary to burns, which is not apparent at
the beginning. Factors involved in edema development are burn size & depth, burns to head
& face, inhalational injury, associated trauma or burns inside mouth. Children at higher risk
to develop airway injuries. Physical signs indicated possibility of upper airway edema
development are signs of inflammation, mucosal injury, soot in pharynx, and edema.
Indications of early intubation are :
◦ Airway obstruction signs: Hoarseness, stridor, accessory respiratory muscle use, sternal
retraction
◦ Extent of burn: >40-50% of total body surface area
◦ Extensive and deep facial burns
◦ Burns inside mouth
◦ Significant edema or risk of edema
◦ Difficulty swallowing
◦ Signs of respiratory compromise: Inability to clear secretions, respiratory fatigue, poor
oxygenation and ventilation
◦ Decreased level of consciousness
◦ Transfer of patient with large burns and airway issue without accompanying competent
personnel
◦ Carboxyhemoglobin level >10%
◦ Circumferential burns of neck.
• Breathing & ventilation: 3 main issues are involved with burns that are of hypoxia, carbon
monoxide poisoning and inhalational injury.
◦ Hypoxia: From inhalational injury, circumferential chest burns, or thoracic trauma. Tt:
Supplemental oxygen.
 ◦ Carbon monoxide poisoning: Always assumed in burns case, Dx based on h/o exposure
and measurement of carboxyhemoglobin. Levels <20% are asymptomatic, higher CO
levels present mainly with headache, confusion, coma & death. Cherry red
discolouration is rare sign in moribund patients. CO has high affinity for Hb and slowly
dissociates with a half-life of 4 hrs, which gets considerably reduced to 40minutes if
patient has been breathing 100% Oxygen hence the Tt strategy of giving 100% oxygen
at NRBM mask. Dx is confirmed by measuring carboxyhemoglobin levels or on
cooximetry, if it cannot be confirmed then empiric treatment with 100% O2 can be
given.
◦ Cyanide poisoning: Can co-occur with CO poisoning, it presents as persistently
profound unexplained metabolic acidosis.
◦ Inhalational injury: Caused by inhalation of carbon particles and toxic fumes that settle
down in terminal bronchioles where they damage the mucosal cells causing capillary
leakage leading to increased fluid requirements and oxygen diffusion defect. The
resulting necrotic cells may slough off from airway linings and clog the airway,
diminished clearance of which produces plugging, increasing the risk of pneumonia
which early on is caused by penicillin resistant Staphylococcus aureus & 5-7 days later
is caused by Pseudomonas aeruginosa, the debris can also cause distal barotrauma by
acting as a ball valve that opens in inspiration and closes during expiration,
accumulating additional volume of air which adds pressure culminating in
pneumothorax & decreased lung compliance. There are 2 requirements to Dx, one is
exposure to combustible agent and signs of exposure to smoke in lower airways below
vocal cords on laryngoscopy. The likelihood of inhalational injury is more with burns
cases in enclosed space with prolonged exposure alongwith O/E finding of
hoarseness,wheezing and carbonaceous sputum. Worsening of chest X-ray and ABG
values supports diagnosis & it’s confirmed on bronchoscopy showing findings of airway
erythema, ulceration & prominent vasculature in addition to infra-glottic soot.
Tt: Patients with >20% TBSA should be intubated empirically any full thickness burns
of anterior and lateral chest walls should be removed with escharotomy. Antibiotics for
methicillin resistant staph and pseudomonas should be considered empirically at 1st sign
of infection, Nebulized heparin to dissolve necrotic debris casts, in children it is given
with added N-acetyl cysteine which improves reintubation & mortality rates.
Hypertonic saline to induce coughing and racemic epinephrine in extubated patients.
High frequency percussive ventilation strategy in which standard tidal ventilations and
respirations is combined with high frequency respirations.
• Circulation: Fluid losses are ongoing due to capillary leakage from inflammation. Fluid
resuscitation for deep partial and full-thickness burns larger than 20% TBSA. Warmed
crystalloid solutions are used. Longer catheter lines are used over traditional lines because of
risk of dislodgement of catheter due to edema. Fluid rate calculated using parkland’s
formula (TBSA*weight*4=volume, 1st half in 8hrs last half in 16). ECG should be done in
suspected rhythm cases as they are common from hypoxia or electrolyte disturbances.
Lactated ringer’s without dextrose in adult and with dextrose in children <2y/o.
Secondary survey
• Total body surface area burned: Based on rule of 9s, TBSA of apart based on multiples of 9,
in adults, each lower limb, anterior and posterior each is 9%, torso anterior and posterior
each is 18%, each upper limb anterior and posterior each are 4.5% and head anterior and
posterior each is 4.5%, same is in infants except the lower limb each anterior and posterior is
7% and back of torso is 13% and each buttocks are 2.5%. Palmar surface either in infants
and adults is considered 1%.
• Depth of Burns:
◦ Superficial 1st degree burns: Characterized by erythema and pain, and they do not blister,
epidermis remains intact,. they are not life threatening and do not require fluid
resuscitation. E.g sunburns or minor kitchen scalding. Tt involves analgesia
◦ Partial thickness: Characterized as superficial partial thickness or deep partial thickness.
▪ Superficial partial thickness injuries are no deeper than papillary dermis they present
with loss of epidermis (producing blisters) these burns are moist, painfully
hypersensitive even to air current, potentially blistered, homogenously pink, little to
or no capillary staining and blanch to touch,hair follicles remain intact which O/E
appears as retention of hair on gentle traction E.g in kitchen scalding injury or flash
flame burns. Heal without residual scarring within 2 weeks because of intact
epidermal structures in rete ridges. Conservative Tt
▪ Deep partial thickness involve deeper parts of reticular dermis, clinically epidermis
is gone, they are drier, less painful, insensate esp. Difficulty to differentiate sharp
from blunt pressure when examined with needle, potentially blistered, red or mottled
dermis, abundant fixed capillary staining and do not blanch to touch. Deep dermal
burns takes 3 or more weeks to heal without surgery and produces severe
hypertrophic scars.
◦ Full thickness burns: Hard, Leathery, skin may appear translucent or waxy white to
charred black, anaesthetic to touch or on pinprick, and generally dry, epidermis is
removable and when removed underlying dermis may be red initially, but does not
blanch with pressure, this dermis is also usually dry and does not weep, No capillary
return. The deeper the burn the less pliable and elastic it becomes, hence appearing
swollen.
• Gastric intubation for nausea & vomiting, abdominal distention or involvement of >20%
TBSA. Feeding should be started within 6 hours of injury to reduce gastric damage. Burns
are catabolic in nature which continues till the wound is present necessitating rapid excision
of burns and stable coverage of wound. Patient’s energy expenditure reduced by keeping
them in warm environment and excess energy requirements provided with nutritional
balance monitored by measuring weight and nitrogen balance.
 • Gut changes: Microvascular damage and ischaemia to gut, Reduces gut motility and prevent
food absorption. Failure of enteral feeding is a life threatening complication. Gut
translocation of enteric bacteria is a source of infection. Gut mucosal swelling, gastric stasis
and peritoneal edema can cause abdominal compartment syndrome.
• Circumferential full thickness burns around limbs act as tourniquet as limb swells
progressing to life threatening limb ischemia.
• Immunodeficiency due to decrease CMI, prone to opportunistic bacterial (e.g MAC
pneumonias) or fungal (candidiasis or cryptosporidiosis). Infections of gut, lung and
monitoring lines and catheters (central line, foley’s) is common. Control infection with hand
wash. Due to catabolic nature of burns hypothalamus sets tempeterature abvoe 37 C, hence
temperature significant to be called fever are those above 38.5 C/101.3F, but other signs of
infection are more useful like rise or fall of WBC count, thrombocytosis, increased sign of
catabolism and worsening patient status. A basic surveillance of patient’s normal flore ais
done from central lines and other areas and culture is sent for suspected case based on which
antibiotics started.
• Awareness for compartment syndrome: Pain out of proportion, diminished peripheral pulses,
tense swelling and pain on passive stretch of muscles.
• Analgesia: Restlessness from hypoxia or hypovolemia rather than pain, hence those r/o’d or
managed 1st than administering narcotics. If pain is really the cause then simply covering the
wound reduces pain a lot, topical cooling also helps. In large burns narcotics or sedatives
have to be administered they have to be done so in small frequent dose with IV route only,
short burst of it requires just before dressing change. IM & subcutaneous route should not be
preferred in patients with TBSA >10% as absorption is unpredictable and dangerous owing
to peripheral vasoconstriction.
• Psychological: Intrusive reactions, arousal reactions and avoidance reactions.
• No prophylactic antibiotic uses only if any signs of infections.
Burns management
• Any deep partial thickness or full thickness burn wound except those that are less than
4cm2, need excision and grafting within 48 hrs or risk of sepsis and multiple organ
dysfunction. Any burn of intermediate depth should be reassessed after 48hrs, because burns
appearing superficial may well deepen over time
• Reconstruction: Done if contractures occur, in early healing period acute contractures 1 st
develop around eye predisposing to exposure keratitis and eyelids must be grafted at 1st sign
of difficulty closing eyes. Other areas can hae delayed recontruction esp. In large full
thickness burns. Burn alopecia Tt with tissue expansion of unburnt region.
• Escharotomy: Especially if developing compartment syndrome. Complication of this
procedure is hypotension from blood loss or release of anaerobic metabolite., if distal
perfusion not improved then suspect central hypotension.
• Full thickness wounds and deep dermal wounds: Dressings with salves, soaks or antibiotic
containing dressings. Salves lose potency continuously till next dressing change requiring us
to change dressing, which itself damages and denudes the wound tissue. Soaks are
chemicals used to completely soak the dressing into, their action is retained for a long time
and it can be added on pre-existing dressing without changing it, however it macerates the
skin or graft covered by dressing, antibiotic dressing has longer duration of action without
reuiring constant change, however it needs to be kept moist and thus need monitoring.
◦ Salves: 11% mafenide acetate, 1% silver sulfadiazine, polymyxin B, neomycin,
bacitracin and mupirocin and the antifungal nystatin.
▪ 11% mafenide acetate: Good against Pseudomonas & Enterococcus species, also it
can penetrate eschar not possible by silver sulfadiazine, problem with it is painful
topical application, allergic skin reaction and it is a potent carbonic anhydrase
inhibitor thus application over large area can lead to metabolic acidosis, hence it is
reserved for small full thickness burns.
 ▪ Silver sulfadiazine: good against gram positives, most gram negatives and some
fungals, some Pseudomonas possess plasmid mediated resistance, it is painless on
application but necessitates frequent dress change producing pain, some may
complain on burning sensaton on application, transient leukopenia develops over 3-5
days of use and it resolves on its own.
▪ Petroleum based antibiotics like polymyxin B, neomycin and bacitracin are painless,
clear on observation allowing easy wound observation, and used for treatments of
burns on face, graft sites and local donor sites and small partial thickness burns.
Mupirocin is particularly good for methicillin resistant Staph aureus, and nystatin for
fungal.
◦ Soaks:
▪ 0.5% silver nitrate: Produces black or dull gray staining of surrounding structures
when it dries, interfering in deciphering the burn wound depth during burn excision.
It is also a hypotonic solution and its continous use can lead to electrolyte leaching
and rarely methaemoglobinaemia.
▪ 0.05% Dakin’s solution (sodium hypochlorite with buffers) is good against most
microbes but also cytotoxic to patient’s healing tissue.\
▪ 5% Mafenide acetate
◦ Antibiotic dressings: Nanocrystalline silver dressings, need to remain moist and thus
require monitoring:
▪ Silver sulphadiazine: Good against Pseudomonas and MRSA
▪ Silver nitrate: Good against Pseudomonas,
▪ Mafenide acetate: Commonly used in USA, produces metabolic acidosis.
▪ Silver sulphadiazine with cerium nitrate: Hard effect on burns converting them into
sterile eschar, good for conservative management. Preserves CMI esp. In elderly.
• Superficial partial thickness and mixed thickness wounds: They heal on their own, requires
dressings that are easy to apply, non painful reduce pain, simple to manage and locally
available. The burn need exposure i.e changing the dressing daily with topical antibiotics,
cotton gauze and elastic wraps till eschar forms which then separates as wound
epithelialises.
Hydrocolloid dressings uses esp. For mixed depth burns, as they contain high amount of
protease aiding in debridement of deeper areas of burns. They also provide moist
enviornment.
Early debridement and grafting is key to effective treatment in most deep partial and full
thickness burns.
• Superficial burns do not require dressing and can be managed with topical salves and
analgesia.
• All burns cause swelling which can be reduced using elevation, splintage and exercise. All
of which need to be started on day 1.
• Feeding: Enteral feeding is mainstay, it may lead to complications like mechanical
obstruction, enteral feeding intolerance and diarrhea. Parenteral feeding done if patient can’t
tolerate enteral feeding.
• Hypertrophic scars: pressure garments for 6-18 months. At locations difficult to apply
garments or smaller locations, silicone patches to speed scar maturation or intralesional
injection of steroid. Itching an dermatitis is a common complication
• Minor burns:
◦ Blisters: May be left alone or removed, but don’t leave a ruptured blister
◦ Wash burn wounds with chlorhexidine
◦ Dressing with nonadherent vaseline soaked gauze or mepitel. These burns heal by 7-
10days. Silver sulphadiazine 1% also used for minor burns except in pregnant, nursing
moms and infants ,2m/o as it causes kernicterus in these patients.
 ◦ Infection in minor burns should be aggressively managed, as infections in superficial
burns to partial thickness to a deep thickness burns. It should be managed with topical
and systemic agents. Debridement and skin grafting should also be considered.
◦ Itching: Common on burn wounds and resultant scar, Histamine and various
endopeptides are involved. Antihistamines, analgesics, moisturizing creams, aloevera
and antibiotics have all been tried with varying success.
◦ Healed burn wounds are prone to blisters from trauma, due to very fragile epithelium,
non-adherent dressings usually suffice, regular moisturizer are also effective.
Complications and management
• Sepsis and multiple organ dysfunction
• Individual organ dysfunction:
◦ Renal failure: can happen during resucitation of 7-14 days later with hypervolemia,
hyperkalemia, metabolic acidosis and oliguria/anuria, managed with maintaing the urine
output and dialysis in severe cases.
◦ Pulmonary failure: Managed with early extubation
◦ Hepatic failure: Replacing factor levels and albumin
◦ Hematologic failure: in 2 ways, loss of coagulation factors and thrombocytopenia, DIC
caused by degradation of blood brain barrier and exposure of brain lipids to plasma.
Managed with Fresh frozen plasma & cryoprecipitate.
Unique burns and management
• Chemical burns: Alkali burns more dangerous than acidic. Acidic burns coagulate and
decreases further penetration into body whereas alkali burns liquidate and increase their
penetration into body. Most chemicals are flushed with large quantities of warmed water for
atleast 20-30 minutes or more if suspected alkali, only in phosphorus burns and elemental
sodium burns they are removed with forceps or a brush. Don’t use neutralizing agents due to
possibility of exothermic reaction and further burning. Alkali burns to eye require continues
irrigation during 1st 8 hrs using morgan lens, small caliber cannula can be fixed in palpebral
sulcus.
◦ Specific acid burns:
▪ Hydrofluoric acid burns require specialized burn units, fluoride ions systemically
cause calcium & magnesium chelation producing hypocalcemia & hypomagnesemia
that can result in arrythmias the hydrogen released by acid causes dehydration and
tissue corrosion, initially treated with topical calcium gluconate gel these burns are
initially very painful because of calcium chelation and potassium release, this finding
can be used to determine efficacy of treatment, the gel should be changed every 15
minutes till pain subsides, if incomplete pain relief after several applications or
symptom recurrence then intradermal injection of calcium gluconate given,
intrarterial may also be given, if not treated then decalcification of bones and
extension of soft tissue may happen. Severe Burn wounds or burns to large area of
limb requires beir’s block (intravenous regional anaesthesia, usually given in
surgeries of upper and lower limb <1hr long) with 10% calcium gluconate. Burns
from acid concentration >50% can cause hypocalcaemia & subsequent arrhythmias
which is an indication for acute early excision. Alll patients with hydrofluoric acid
burns should receive cardiac monitoring for QT prolongation, calcium gluconate
should be added into resuscitative fluids, and serum electrolytes monitored and
electrocardiographic changes should institute rapid response with IV calcium
chloride.
▪ Formic acid burns: Used in industrial limescale descaling and as a hay preservative.
Sustained formic acid exposure produces electrolyte abnormalities like metabolic
acidosis, renal failure, intravascular haemolysis and pulmonary complications.
Acidemia detected on ABG should be corrected with IV bicarbonate. Haemodialysis
indicated when extensive formic acid absorption. A formic acid wound is typically of
 greenish appearance and deeper than initially appears, it is best treated with by
surgical excision.
◦ Specific alkali burns:
▪ Concrete burns (calcium oxide): Occurs in construction workers with hours of
contact with cement, predominantly involving the lower limb in areas around ankle,
underneath boots, knee or foot. Critical substance responsible is hydroxyl ion.
Cement also produces exothermic reaction when in contact with perspiration. Tt
involves removal of clothing, irrigating area with soap and water, until all cement
removed and effluent has a pH of less than 8. Injuries tend to be deep because of
exposure times and surgical excision and grafting of resultant eschar may be
indicated.
• Electric burns: Electricity produces heat when transmitting through human body which acts
as a volume conductor, due to varying rates of heat loss from superficial and deep tissues,
deeper burns can coexist with relatively normal looking skin, hence electric burns are more
serious than they appear. Electric current may travel through nerves \and blood vessels
causing nerve injuries and thrombosis. Rarest and the worst form is in pediatric patient’s
electric oral commissural burns caused by child chewing on ends of a live wire and
electricity being conducted through their saliva burning their mouth commissure, the
resultant sequale involves development of scarring and contractures around mouth
producing microostia and difficulty feeding.
Severe injuries typically presents with contracted hand with small electrical entrance wound,
alerting for deeper soft tissue injury more extensive than obvious.
Electricity can cause cardiac arrest producing dysrythmias, prolonged monitoring is reserved
only for cases of demonstrable electric burn injuries, loss of consciousness, exposure to high
voltage, or cardiac rhythm abnormalities, or arrhythmias on early evaluation.
Assess for possibility for fractures esp. of spine common due to electricity induced muscle
contractures.
Rhabdomyolysis is assumed and if patient pees dark red urine institute empiric management
for myoglobinuria that is fluid resuscitation till urine depigmented and then later to maintain
normal urine output.
• Tar burns: Very hot till 450F and sticks to skin and clothes resulting in continued heat
transference. Tt rapid cooling of tar and then careful removal, best method is using mineral
oils for tar removal.
• Ionising radiation: can be classified into 2 groups, whole body or localized.
◦ Localized radiation: Conservative management until true extent of injury found out. If
such a radiation causes ulcer, that is managed with excision and coverage with
vascularized tissue.
◦ Whole body radiation: Can be lethal or non lethal. Lethal is characterized by presence of
acute desquamation, whereas a non lethal is characterized by gut mucosa symptoms &
immune dysfunction. Management is supportive and giving iodine tablets.
• Hydrocarbons: Dissolves cell membranes and causes cell necrosis. Superficially it produces
erythema and blistering, if absorbed systemically, it produces respiratory depression and
hepatic injury, thought to be a/w benzenes. Ignition of hydrocarbons produces deep full
thickness burns.
• Abuse: Characteristic burn patterns indicating abuse
◦ Circular burns
◦ Burns with clear margins
◦ Uniquely patterned burns
◦ Burns on sole of child’s feet: Happens when immersing in hot water
◦ Burns on posterior aspect of lower extremity and buttocks in elderly with soaking in hot
water
◦ Old burn injuries in setting of new traumatic injuries like fracture.
Cold Injuries
• More severe with lower temperatures, immobilization, prolonged exposure, moisture, and
presence of peripheral vascular disease and open wounds.
• 2 types Non freezing injury and frostbite.
Frostbite
• Damage due to tissue freeze or ice crystals injuring cell membrane, blocking micro-vessels
and causing tissue anoxia. Some damage contributed to reperfusion injury with rewarming.
Classified into degrees based on depth of involvement, be aware: not good for
prognostication.
◦ 1st degree: Only hyperemia and edema. No skin necrosis
◦ 2nd degree: hyperemia & edema accompanied with large clear vesicle formation with
partial-thickness skin necrosis.
◦ 3rd degree: full thickness skin necrosis with subcutaneous necrosis and hemorrhagic
vesicles
◦ 4th degree: Full thickness skin necrosis with muscles and bone
• Affected part cold, hard, white and numb initially which changes with treatment course.
Common initial treatment. Definitive surgical treatment depends on when level of
demarcation appears in the perfused tissue which might take weeks to months to reach a
final stage.
Non freezing injury
• Trench foot or cold immersion foot describes such injuries. Happens with exposure to
temperatures just above freezing (1.6 C-10C or 35F-45F) Commonly seen in soldiers,
sailors, fishermen and homeless.
• Pathophys: Microvascular injury stasis and vascular congestion
• Foot appears black but no actual underlying tissue necrosis
• Alternating arterial vasospasm and vasodilation with affected tissue 1st cold and numb then
progress to hyperemia within 24-48hr, with hyperaemia comes intense pain, painful burning
and dysesthesia and tissue damage characterized by edema, blistering, hyperemia,
ecchymosis and ulcerations
• Injury complicated by infections such as cellulitis, lymphangitis, and gangrene, which can
be prevented with proper foot hygiene.
Management of cold injuries
Divided into 3 phases, rewarming, local wound care and definitive management
• Rewarming:
◦ ASAP to decrease duration of tissue freeze
◦ Not attempted if risk of refreeze.
◦ Not attempted if patient presents with clearly dead blackened body parts.
◦ Replace constricting damp clothes with warm blankets and administer warm fluids
orally if patient able to drink.
◦ Place injured part in circulating water at constant warm (40c/104F) Temperatures till
perfusion returns as seen with pinkish colouration of tissue usually in 20-30 minutes.
◦ Best done in setting with large tank, such as whirlpool tank, or placing injured limb in a
bucket with warm water running in.
◦ Excess dry heat may cause burn injury as limb is insensate.
◦ Rubbing or massaging area not done.
◦ Rewarming extremely painful and adequate analgesics like IV narcotics required.
◦ Warming areas produces large reperfusion syndromes with tissue edema, acidosis and
hyperkalemia requiring cardiac status and peripheral perfusion monitoring.
• Local wound care
◦ Goals are preventing infection, avoiding opening uninfected vesicles, and elevating
injured area.
◦ Protect affected site by cradle or tent
 ◦ Avoid pressure on affected site
◦ Keep wound clean, leave uninfected nonhemorrhagic blisters intact for 7-10 days
◦ Tobacco, nicotine and vasoconstrictors to be stopped.
◦ Minimize weight bearing at affected part.
• Definitive management
◦ Local wound care with topical antiseptic dressings & observation for weeks to months
till clear line of demarcation b/w dead and living tissue appears which helps in
estimating the depth and extent of tissue injury.
◦ Surgical debridement of dead tissue.
◦ Early surgical debridement (before demarcation) and amputation only if severe
infections appear.

Pediatric injury

General points
• Prone to multi systemic injury because of smaller body mass resulting in impaction of
greater force per unit body area, such force is resisted by a body that has less fat, less
connective tissue & closer proximity of multiple organs than in adults.
• Prone to head injury resulting in hypoxia, apnea and hypoventilation requiring aggressive
airway management v/s hypovolaemia & hypotension in adult.
• No. 1 cause of mortality is motor vehicle accidents
• Child maltreatment is no. 1 cause of homicides in children <12 months
• Firearm injuries are no. 1 cause of homicide in children >1y/o
• Majority of kids won’t deteriorate while treatment and have no haemodynamic abnormality
only some may have deteriorating haemodynamics and may develop complications.
• Also prone to develop hypothermia due to greater ratio of body surface area to body mass.
• Have more pliable and incompletely calcified skeleton as compared to adults, so can sustain
injuries severe enough to damage internal organs but leave skeleton unaffected e.g no rib
fracture in a kid with pulmonary contusion. If a child sustains rib or skull fractures then it
suggests transfer of a very massive amount of energy and underlying organ injuries like
brain or lung contusion should be assessed for.
• Child uses regression as a defence mechanism.
• Lifelong disabilities occur as a result of injuries crossing through the growth plate, femur
involvement results in leg length discrepancy interfering in running and walking, thoracic
vertebral growth plate involvement results in kyphosis, scoliosis or gibbus deformities,
massive disruption of spleen requires splenectomy and predisposes child to overwhelming
post splenectomy sepsis and death.
Primary survey
• Airway: 1st priority, frequently inability to secure a patent airway with resulting hypoxia and
hypoventilation results in cardiac arrest.
◦ Child has its neck in partial flexion, this buckles posterior pharynx anteriorly interfering
with intubation, to prevent this child should be layed supin one spine board with its
plane of midface parallel to spine board.
◦ Several anatomical features interfere with intubation like soft tissue of child’s
oropharynx, which are larger compared to other structures in oral cavity, compromising
visualization, child’s larynx being funnel shaped allowing secretions accumulating in
retropharyngeal area, larynx and vocal chords being more cephalad and anterior in neck.
The vocal cords being more difficult to visualize in normal position compared to neutral.
◦ Infant’s trachea is shorter and results in displacement of intubation in right mainstem
bronchus, inadequate ventilation, accidental tube dislodgement and mechanical
barotrauma adequate depth of intubation is 3 times the appropriate tube size.
 ◦ Intubation process involves placing child in neutral position, holding cervical spine,
opening mouth by jaw thrust, clearing suction and debris, fully preoxygenating the child
and then attempting intubation.
◦ Oropharyngeal airway is not placed upside down and rotated 180 degress due to risk of
injuring oral soft tissues, instead it is carefully placed into oropharynx normally with a
tongue depressor.
◦ Orotracheal intubation is performed for child with brain injuries requiring controlled
ventilation, child in whom airway can’t be maintained, child exhibiting respiratory
failure and those who have suffered significant hypovolemia leading to sedepressed
sensorium or operative intervention.:
▪ The cricoid ring in child forms a natural ring around uncuffed ET tube so dont requir
inflating cuff.
▪ Appropriate size of ET tube is equal to diameter of child’s external nares or tip of
child’s smallest finger
▪ Infants have more pronounced vagal response to intubation than children or adults,
and may experience bradycardia with direct laryngeal stimulation, however any
bradycardia in these subsets is more likely due to hypoxia than laryngeal stimulation.
Atropine sulfate should be given in such cases and it helps in drying up secretions
allowing clear vision.
▪ Nasotracheal intubation is not performed in kids due to possibiltiy of injuring the
cranial vault or the nasopharynx
▪ Position of ET tube is assessed by auscultating both hemithoraces to ensure no right
mainstem bronchus intubation, then seondary confirmatory device like real time
waveform capnograph, colorimetric end tidal CO2 detector or esophageal detector
device.
▪ Because young kids have small trachea any head movement displaces ET tube,
inadvertent extubation, right mainstem bronchus intubation or vigorous coughing
due to irritation of carina by the tips. An these complications may not be identified
till they have worsened a lot, Hence clinicians need to monitor breath sounds
periodically.
▪ If any doubt about incorrect placement, that canot be resolved quickly, then remove
the ET tube, “don’t be a DOPE” is usemful mnemonic (D- dislodgement, O-
Obstruction, P-Pneumothorax and E- equipment failure)
◦ If airway intubation cannot be achieved with bag and mask ventilation or orotracheal
intubation, a laryngeal mask airway, intubating LMA or needle cricothyroidotomy is
necessary. Surgical cricothyroidotomy is rarely indicated.
• Breathing:
◦ Adult sized bag and mask not used as it causes barotrauma, use of pediatric sized bag
and mask for children <30kg.
◦ Hypoxia is most common cause of cardiac arrest, and respiratory acidosis most common
acid-base abnormality caused by hypoventilation both of which can be resolved with
adequate ventilation and perfusion, in absence of adequate ventilation, attempting to
correct acidosis with sodium bicarbonate worsens acidosis and causes further
hypercarbia.
◦ Penumothorax to be managed with needle thoracotomy at 2nd intercostal space and the
chest tube placement by tunneling.
• Circulation
◦ Children have increased physiologic reserves and present normally even in shock.
◦ Upto 30% decrease in circulating blood volume may be required to manifest a decrease
in systolic BP.
 ◦ Tachycardia and poor skin perfusion may be the only keys to early recognition of
hypovolaemia, of which tachycardia may also be present if child is afraid, in stress or
fear.
◦ Other subtle signs of hypovolaemia is diminished pulses, narrow pulse pressure
<20mmhg, mottling of skin (clammy skin in infants in young child), cool extremities
compared to torso, decrease in level of consciousness and dull response to pain.
◦ BP and urine output should be continuously monitored although they worsen in late
stages. Mean Systolic BP is 90mmhg + twice child’s age in yrs and lower end of systolic
BP in kid is 70 mmhg + twice child’s age in years. Diastolic BP is 2/3rds of systolic BP.
◦ Hypotension in child represents a state of decompensated shock indicating severe blood
loss of >45%. tachycardia changing to bradycardia often accompanies this hypotension
which may occur suddenly in infants, to prevent this a rapid infusion of both isotonic
crystalloid and blood must be given.
◦ After weight based dosing of resuscitative fluids if child demonstrates ongoing bleeding
after 2nd or 3rd dose then PRBC is given, but a trend of starting PRBC just after initial
bolus of crytalloid is also being practiced. Return to normal is suggested by slowing of
heart rate, clearing of sensorium, return of pulses, return of normal color, increased
warmth of extremities, increased SBP to age appropriate normal, increased Pulse
pressure, urinary output 1-2ml/kg/hour.
◦ Transient and non responders (similar definition as adults) are candidates for additional
blood transfusion and massive transfusion protocol.
◦ Thermoregulation: child’s thin habitus & skin, less subcutaneous fat, predispose to heat
loss,. Hypothermia can compromise response to treatment, prolong coagulation time and
adversely affect CNS function. Overhead lamps, heaters and thermal blankets to
preserve body heat. Warm the room as well as the IV fluids, blood products and inhaled
gases.
Secondary survey
• Thoracic trauma
◦ 80% injuries occur in chest.
◦ Chest injury a marker for any further multi systemic injury.
◦ Most common mechanism is blunt injury, the pliability or compliance allows kinetic
energy to transmit to underlying structure like the pulmonary parenchyma causing
contusion.
◦ Mobility of mediastinal structures places children at increased risk of tension
pneumothorax, managed the same way as in adults.
◦ Penetrating injuries more common after 10y/o.
◦ Most injuries identified on X-ray, no need for cross section at CT.
◦ Most cases appropriately managed with supportive care and tube thoracostomy.
• Abdominal trauma
◦ Most cases caused by falls or motor vehicle accidents, hypotensive cases require prompt
surgical intervention
◦ Don’t apply deep palpation during examination as it may cause voluntary guarding due
to pain.
◦ Most children when stressed ingest large amount of air, which causes upper abdominal
distension confusion examination. Oro gastric decompression to relive the distension.
◦ Presence of shoulder and/or lap belt marks suggest intrabdominal injuries, especially in
presence of lumbar fractures, intraperitoneal fluid and persistent tachycardia.
Decompression of urinary bladder facilitates examination.
◦ Diagnostic adjunct:
▪ CT scan: used with radiation kept as low as reasonably achievable (ALARA), to
keep it so CT is done only when absolutely medically necessary to prevent
 irradiation of child. Scan only if management changes significantly, scan only area of
interest and using the lowest possible radiation dose.
▪ FAST: Should not be used to rule out abdominal injuries. Even without any
intraperitoneal fluid, significant injuries may be present. FAST can identify small
amount of intraperitoneal fluid that is unlikely to be associated with significant
injuries, if that amount is larger then then a serious injury is more likely. Operative
management depends not on the amount of intraperitoneal fluid but by hemodynamic
abnormality and its response to treatment. FAST is also incapable to identify
intraparenchymal injury. If a small amount of intraperitoneal fluid is present in
hemodynamically normal child then obtain a CT.
▪ Diagnostic peritoneal lavage (DPL). Done when hemodynamically abnormal that
child cannot get a CT and there is no FAST modality & the presence of blood would
require immediate surgical intervention. DPL only useful to diagnose intraperitoneal
viscera only not retroperitoneal injuries. Only the surgeon who will ultimately treat
the child should do the DPL.
▪ Management:
• Conservative: Done for the hemodynamically stable
◦ Hemodynamically stable and negative CT or FAST are candidates.
◦ Presence of positive finding in CT/FAST,grade of injury or presence of
vascular blush does not necessarily mean laparotomy.
◦ Bleeding from injured, spleen, liver or kidneys is self limited, thus positive
FAST/CT does not mandate laparotomy is child stable or responding to
fluids.
◦ For conservative management ICU is must, in resource limited setting do
surgery.
• Surgical management: Done if hemodynamically unstable or not responding to
fluids and diagnostics like CT/FAST positive for blood. Choice of operation is
laparotomy and it is used to control hemorrhage.
• Specific visceral injuries: Certain injuries much more common in children than
adults.
◦ Injuries like striking bicycle handlebars, getting elbowed in upper quadrant
and lap belt injuries are common and result in viscera getting compressed b/w
the blow and the spine posteriorly.
◦ Blunt pancreatic injuries are caused by above such mechanism & its
management depends on injury extent.
◦ Small bowel perforation at or near the ligament of treitz are more common in
children than adults as are mesenteric and small bowel avulsion injuries, such
injuries are diagnosed late because of vague nature of presentation.
◦ Bladder rupture is also common in kids because of shallow depth of pelvis.
◦ Children restrained by lap belt, only are at particular risk of for enteric
disruption especially if they have belt marks over their abdomen or they have
chance fracture of lumbar vertebrae, any such patients should be assumed to
have risk of intraabdominal injuries until proven otherwise.
◦ Penetrating injuries of perineum, straddle injuries may occur with fall onto
prominent object and result in intraperitoneal injuries due to proximity of
peritoneum to perineum.
• Head trauma
◦ More prone for momentum induced head injury, because subarachnoid space is
relatively smaller and hence less buoyant offering less protection to brain.
◦ Normal cerebral blood flow increases nearly twice that of adult levels by age of 5 years
and decreases, this accounts for children’s significant susceptibility to cerebral hypoxia
and hypercarbia.
 ◦ Assessment:
▪ Outcome of head trauma is better in kids compared to adults, outcomes are better in
older child compared to ,3y/o. Outcomes affected by hypotension caused by
hypovolemia and hypoxia resulting in secondary brain injury. Hypotension from
hypovolaemia is single biggest risk factor, critical to ensure adequate and rapid
restoration of an appropriate circulating volume.
▪ Infants can experience significant hypotension due to bleeding into subgaleal,
epidural and intraventricular spaces because of infant’s open cranial sutures and
fontanelles, in such cases treatment focuses on appropriate volume restoration.
▪ Open fontanelles and mobile cranial sutures can tolerate expanding cranial mass
lesion or brain swelling and signs of these conditions may be hidden until rapid
decompensation may occur. An infant not in coma, but who has bulging fontanelle
and suture diastases should be assumed to have more severe injury requiring
neurosurgical consult.
▪ Vomiting and amnesia are common after injury but don’t necessarily mean increased
intracranial pressure. Only persisting vomiting or that which become more frequent
is a concern and mandates CT of head.
▪ Impact seizures or seizures occurring shortly after brain injury are more common in
children and are usually self limited, all seizures activity should be investigated by
the CT scan.
▪ Children have fewer focal lesion than adults but more commonly have raised
intracranial pressure due to swelling. Rapid restoration of circulating volume is
priority.
▪ GCS score is useful to monitor clinical condition, although in children the verbal
component is slightly modified:
• Appropriate words or social smile, fixes and follows- 5
• Cries but consolable- 4
• Persistently irritable- 3
• Restless, agitated-2
• None-1
▪ Because increased intracranial pressure frequently develops in children,
neurosurgical consult, to consider intracranial monitoring early in resuscitation
should be considered in following cases:
• GCS <8 or motor component 1 or 2.
• Multiple injuries associated with brain injuries requiring major volume
resuscitation, immediate lifesaving thoracic or abdominal surgery or for which
stabilization and assessment is prolonged.
• CT scan of brain, that demonstrates evidence of brain haemorrhage, cerebral
swelling or transtentorial cerebral herniation. Management of intracranial
pressure is integral to optimize CPP.
◦ Management:
▪ Management of ABCDEs as mentioned above, in particular prompt airway
management.
▪ Hypertonic saline or mannitol to decrease intracranial pressure.
• Spinal cord injury:
◦ Most commonly caused by motor vehicle crash or sporting injuries.
◦ Children commonly have pseudosubluxation of C2 on C3, which appears more
pronounced when child lies supine on hard surface, it is corrected by placing a 1 inch
layer of padding beneath the entire body from shoulder to hips, but not the head, and
repeating the X-ray. A true subluxation will not disappear with this maneuver, mandating
further evaluation.
 ◦ Cervical spine injury can be identified on neurological exam findings and detection of an
area with soft tissue swelling, muscle spasm, or a step-off deformity.
◦ An increased distance b/w the dens and the anterior arch, of C1, Gaps exceeding upper
limit of normal for adult are frequently seen.
◦ Skeletal growth centres can resemble fractures. Basilar odontoid synchondrosis appears
as radiolucent area at the base of dens, especially in kids <5y/o.
◦ Apical odontoid epiphyses appears as separation, on odontoid X-ray usually seen b/w 5-
11 years of age. Growth centres of spinous process can resemble fractures at tip of
spinous process.
◦ Children sustain spinal cord injury without radiographic abnormality (SCIWORA). A
normal cervical spine series can be found in upto 2/3rds children who have suffered
spinal cord injury. If spinal cord injury is suspected based on history or results of
neurologic examination, normal spine X-ray examination is not sufficient to r/o spinal
injury. When in doubt about integrity of cervical spinal cord, assume unstable injury
exists, limit spinal motion and obtain appropriate consult.
◦ Plain radiographs prefered over CT/MRI and the latter not done routinely unless,
inability to completely evaluate the spine on radiographs, delineating abnormality on
plain films and to assess spinal injuries in kids with traumatic brain injuries. CT doesn’t
detect ligamentous injury.
• Musculoskeletal injury
◦ Children’s don’t loose a lot of blood from long bone fractures. So any hemodynamic
instability in setting of a long bone fracture should indicate finding at other location e.g
like abdomen
◦ Children’s fracture heal more quicker and less likely to have non union, this is because
of their thicker and stronger periosteum contributing to stability which also helps in
reduction.
◦ Most common complication is that of physeal arrest, rotational and angular deformities
and long bone overgrowth. Trauma is the most common cause of physeal arrest and it
happens because a bony ridge forms b/w metaphysis and epiphysis.
◦ Repeated attempts to reduce a physeal fracture, may injure the physis and lead to growth
arrest, internal fixation should also not cross physis.
◦ Specific injuries:
▪ Distal radial fracture: Most common fractures in children. Fractures proximal to
growth plate is managed with manipulation under anaesthesia and conservatively, as
puberty approaches fractures treated as adults.
In cases where there is significant displacement of distal radius but intact ulna,
secondary redisplacement is common and thus radisu is held with primary K-wires.
If growth plate is involved it it of salter harris type 1 or type 2, managed with
manipulation and casting.
▪ Supracondylar fracture: Presents with 2 major complications, 1)neurovascular
insufficiency, 2) Rotational deformities. Neurovascular insufficiency develops from
displaced fragment compressing the neurovascular bundles and it is best managed
with early reduction, Rotational deformities are of 2 types, one is along the plane of
joint movement which is better as it corrects satisfactorily and other is rotational
valgus or varus deformities which is worse as it is not obvious initially till arm
achieves full extension that happens months after initial injury.
Minimally displaced supracondylar injury is benign and managed conservatively,
whereas a displaced fracture although after manipulation may appear stable if elbow
is in flexion, it actually is not and it should be held with K wires instead of a flexed
cast.
▪ Lateral condylar fracture: A benign injury that is easily missed and have bad
complications if not detected and managed early. Clinically the clue is lateral
tenderness. The X-ray may show a flake of distal humeral epiphysis above
capitellum as the bulk of fracture lies inside cartilage which has not yet ossified.
However this is an interarticular fracture crossing growth plate, which if displaced or
unstable should receive prompt reduction, failure to do so resulting in nonunion or
malunion with growth plate arrest or if attempting reduction of fracture under direct
vision, may even develop avascular necrosis.

▪ Femoral shaft fracture: Managed with traction. Intramedullary nailing avoided in

girls ,12y/o and boys <14 as it may injure growth plate.
 ▪ Tibial shaft fracture: Unstable is managed with casting, external fixation or nailing or
plating.
• Child maltreatment: Suspected if:
◦ History
▪ Discrepecy b/w history and examination: E.g LOC when falling from bed/sofa,
fractures when playing with kids, fractures in lower extremity in nonambulatory
infant.
▪ Delay b/w time of injury and presenting to clinican
▪ h/o repeated trauma, treated in same or different Eds
▪ h/o of injury varies b/w different caretakers
▪ H/o doctor shopping
▪ Parents noncompliant to medical advise
▪ Implausible injury according to developmental milestone
◦ O/E
▪ Multicolored brusies:At different healing stages
▪ E/o frequent previous injuries e.g healed scars or fractures
▪ perioral injuries
▪ injuries to genitals or perianal region
▪ Long bone fracture in kids <3y/o
▪ Ruptured internal viscera without antecedent blunt trauma
▪ Multiple subdural hematomas without antecedent fresh skull fracture
▪ retinal hemorrhages
▪ Bites, cigarette burns and rope marks
▪ sharply demarcated second or third degree burns
▪ skull fracture or rib fracture seen in children <2y/o
Elderly injury
• General points
◦ Elderly more susceptible to injury due to decreased physiologic reserves, comorbidities
and senescent organs and decreased elastic tissues
◦ Risk of fall increases with age and is most common cause of injury in elderly
◦ Even small to moderate burns, benign in young may cause increased mortality in elderly,
similarly spillage of hot liquid which in younger patients might heal quickly, in elderly
may cause full thickness burns.
• Primary survey: Similar to adults but some nuance in elderly:
◦ Airway: Elderly who lack teeth are easier to intubate but difficult bag and mask
ventilation. If a denture is non obstructing to airway it is kept so for effective bag and
mask ventilation. In edentulous patients a gauze is kept b/w gums and cheeks to achieve
effective bag and mask ventilation. Barbiturates and benzodiazepines dosage is lowered
in rapid sequence intubation.
◦ Breathing: elderly have increased work of breathing due to changes in lungs and chest
wall, and develop respiratory failure, because the heart looses sensetivity to hypoxia
with age, the development of respiratory failure is insidious. Rib fractures are managed
rapidly.
◦ Circulation: Elderly have fixed heart rate and cardiac output, response to hypovolemia
involves increased systemic vascular resistance, since many elderly have modest
hypertension, a normal BP might indicate hypotensive state. A systolic BP of 110mmhg
should be used as a threshold for identifying hypotension in adults >65y/o. An elderly
patient with e/o circulatory failure should be assumed to be bleeding and should be
monitored with CVP, echocardiography and ultrasonography.
◦ Disability: Elderly prone to TBI because of cerebral atrophy, being on anticoagulants or
antiplatelets or having atherosclerotic diseases contributing to primary or secondary
brian injury. Moderate cerebral atrophy may permit intracranial pathology to initially
 present with normal neurologic examination. Degenerative diseases of spine places
elderly patients at risk of fractures and spinal cord injury even with low energy kinetic
falls. Management involves liberal CT usage to identify brain or spine injuries and
reversal of anticoagulant and/or antiplatelet therapy.
◦ Exposure and enviornment: loss of subcutaneous fat, presence of comorbidities,
nutritional deficiencies, premedications puts elderly at risk for hypothermia, reuiring
rapid evaluation and when possible early liberation from spinal boards and cervical
collars to minimize complications.
• Specific injuries: Elderly commonly have rib fractures, traumatic brain injuries and pelvic
fractures:
◦ Rib fractures: Elderly prone to develop rib fractures due to anatomic changes to chest
wall and decreasing bone density with age. Trauma most likely result of fall or motor
vehicle accident. Most common complication is pneumonia. Management is analgesia
and pulmonary hygiene
◦ Traumatic brain injury: Elderly more prone to develop, and have higher risk for
morbidity and mortality and the latter resulting from elderly patient’s inability to
recover. Delirium, dementia and depression are difficult to distinguish from brain injury,
hence liberal usage of CT to delineate any pre-existing conditions and early &
aggressive reversal of anticoagulation using prothrombin complex concentrates, plasma
and vitamin K.
◦ Pelvic fractures: Elderly prone to develop because of linear progression of incidence of
osteoporosis. The fracture is more complicated in elderly frequently requiring blood
transfusions, elderly have much longer hospital stay and fall prevention is mainstay of
management.
• Elderly maltreatment: Signs may be subtle with neglect and poor hygiene or dehydration,
changing history b/w caregivers, discordance b/w history and physical signs. Physical signs
of abuse are:
◦ Bruises at inner arms, inner thighs, ear, mastoid area, buttocks, palms, soles and scalp.
◦ Multiple clustered bruises.
◦ Abrasions to axillary area (from restraints) or the wrist and ankles (from ligatures).
◦ Nasal bridge and temple injuries (from being stuck while wearing sunglasses).
◦ Periorbital ecchymoses.
◦ Oral injury.
◦ Unusual alopecia pattern.
◦ Untreated pressure injuries or ulcer in non-lumbosacral area
◦ Untreated fractures
◦ fractures not involving hips, humerus or vertebra
◦ Injuries in various stages of evolution
◦ Injuries to eyes or nose
◦ Contact burns or scalds
◦ Scalp hemorrhage or hematoma.
OB-GYN injuries
• General points
◦ Two goals mother and fetus. Best initial treatment for fetus is optimal resuscitation of
mother.
◦ Every reproductive aged women should be considered pregnant unless proven otherwise
by definitive ultrasound or UPT.
◦ X-ray examination if indicated should not be held for sole reason of pregnancy.
◦ Early consult with trauma surgeon and an OB-GYN.
• Anatomic changes: Important as they may alter examination finding or alter assessment and
management:
 ◦ Uterus is inside pelvis by 12th week of gestation, then by 20th-24th week it comes
around the umbilicus and by 34-36th week it is at the coastal margins and at 40th week the
fundal height descends to just below the xiphoid because fetal head engages pelvis.
◦ Enlargement of uterus pushes the intestines cephalad, causing them to lie at upper
abdomen, as a result bowel is relatively protected from trauma, whereas uterus and its
contents are more vulnerable, however penetrating trauma to upper abdomen frequently
results in complex intestinal injuries
◦ Clinical signs of peritoneal irritation is less evident in pregnancy.
◦ Because fetal head engages maternal pelvis, fracture of maternal pelvis also result in
skull fracture or serious intracranial injury to fetus.
◦ Unlike elastic myometrium, placenta has little elasticity, this lack of placental elastic
tissue results in vulnerability of sheer forces at uteroplacental interface leading to
abruptio placentae.
◦ Placental vasculature is maximally dilated, yet exquisitely sensitive to catecholamines.
An abrupt decrease in maternal intravascular volume, can result in profound
intravascular resistance, reducing fetal oxygenation despite reasonably normal maternal
vital signs.
• Mechanism of injury:
◦ Blunt injury: Fetus generally protected form this type of injury due to abdominal wall,
myometrium and amniotic fluid, but still suffer direct injury from collision or indirect
from countercoup effect, rapid compression or deceleration effect. In motor vehicle
collisions using lap restraint alone causes the pregnant women to forward flexion and
uterine compression with possible uterine rupture and abruptio placentae, a lap belt worn
too high over the uterus may produce uterine rupture because it transmits direct force to
uterus on impact, hence additional shoulder restraint in pregnant women should be used
as it dissipates deceleration over a greater surface area.
◦ Penetrating injury: Injury more likely to fetus than abdominal viscera.
• Primary survey: Assess & resuscitate mother 1st then assess fetus before conducting a
secondary survey.
◦ Mother:
▪ Airway: Same as adult, ensure patent airway, stabilize C-spine and if inadequate
place an airway oropharygeal, ET tube or if failed a surgical airway.
▪ Breathing: Ensure adequate oxygenation and ventilation. Hypocapnia is
physiological in late pregnancy, A PaCO2 of 35-40mmhg may indicate an impending
respiratory failure during pregnancy.
▪ Circulation: Uterine compression may reduce venous return to the heart aggravating
hypovolemic shock, managed with manually displacing the uterus to relieve pressure
on IVC. Mother may appear haemodynamically stable in hypovolaemia due to
increased plasma volume in pregnancy although the fetus still being in distress due
to decreased perfusion of placenta. Management involves crystalloid infusion.
Vasopressors should be the last resort. Fibrinogen levels should be tested as it
physiologically doubles in pregnancy and normal levels indicate DIC. Maternal
bicarbonate is normally low in pregnancy to compensate respiratory alkalosis.
◦ Fetus:
▪ Main cause of death in a fetus is from maternal shock or death, 2nd main cause of
death is from abruptio placentae.
• Abruption suggested by vaginal bleeding, uterine tenderness, uterine tetany,
uterine irritability (uterus contracts when touched), frequent uterine contractions.
▪ Uterine rupture, suggested by abdominal tenderness, guarding, rigidity, rebound
tenderness and shock, other signs include abnormal fetal lie (oblique or transverse
lie), easy palpationof fetal parts and inability to palpate uterine fundus. X-ray
 evidence includes, extended fetal limbs, abnormal fetal positioning and free
intraperitoneal air.
▪ Perform continuos fetal monitor beyond 20-24weeks of gestation. Patients with no
risk factor for fetal loss should be monitored for 6 hours v/s patients with risk factors
for fetal loss or placental abruption should be monitored for 24 hours. The risk
factors are:
• Maternal heart rate >110bpm
• Injury severity score >9
• E/o placental abruption
• Fetal heart rate >160bppm or <120bpm: fetal heart rate is a sensitive indicator for
maternal blood volume and fetal status. An abnormal heart rate, Absence of
accelerations or beat to beat variability, frequent uterine contractions can be sign
of impending maternal/fetal decompensation.
• Ejection during motor vehicle crash
• Motorcycle or pedestrian collision.
• Secondary survey: Mostly the same as nonpregnant one.Perineum should be evaluated for
rupture membranes, presence of amniotic fluid in vagina evidenced by pH >4.5 suggestive
of chorioamniotic membrane rupture, in such cases cervical effacement and dilation should
be noted. Vaginal exam should be done but not repeated. CT can be performed if concern for
significant intrabdominal injury.
Admission mandatory for uterine pain, irritability, vaginal bleeding, abdominal tenderness,
e/o hypovolemia, changes in or absence of fetal heart sounds and/or leakage of amniotic
fluids
• Management:
◦ If e/o consumptive coagulopathy (from amniotic fluid embolism): Perform uterine
evacuation and replace platelets, fibrinogen and coagulation factors.
◦ All pregnant Rh negative patient should receive Rh immunoglobulin therapy, unless the
injury is distal to uterus.
• Intimate partner violence: Should be screened, substance abuse, bruises over gravid
abdomen, diminished self image, depression, suicidal, inconsistent history, frequent doctor
visits should are signs.
Ocular injuries

• Anatomy
◦ Extraocular muscles attach to globe over sclera in a cone like fashion, this cone is
covered by a fascial sheath called tenon’s capsule, which has minimal distensibility
prohibiting muscles to expand, thus hemorrhage in this area produces compartment
syndrome.
Compartment syndrome can also happen in a space beneath the tendinous attachment to
eyelid medially and temporally by canthal tendons, which normally prevents globe to
move forward.
• Assessment
◦ Time and mechanism of injury
◦ Physical examination:
▪ 3 vital signs of eye:
• Vision: snellens chart and with near vision test card, if patient has refractive error
ask to use glasses or do it via pinhole (if not currently available)
• Pupil: Remove contact lens, Normal- Equal, round, reactive without any afferent
pupillary defect.
Sluggish poorly reactive pupil can be stroke or herniation. Dilated pupil can be
from pupillary sphincter tear due to blunt trauma, past surgery or comorbid
ocular disease (e.g cataracts). Pupils will show some reactivity if lesion localized
to eye only although still be of different sizes.
• Intraocular pressure: Can be roughly estimated by palpating globe with fingers
(tense globe or rock hard globe suggests elevated IOP), precise measurement by
tonometer, should anesthetize eye with topical solution (e.g proparacaine) to
prevent patient excessively blinking or squeezing the eye when using tonometer.
IOP can be erroneously raised with valsalva, mechanical ventilation and
accidental pressure on globe during eye opening.
If open globe is suspected do not check IOP as the act of measurement itself
might drive more intraocular contents outside eye, in such cases check visual
acuity and pupils only.
▪ Anterior segment exam:
• Normal examination: When gently pushing the globe through eyelid, the globe
gives a little and moves backward, when this does not occur, there is resistance to
retropulsion, indicating a possible increased pressure in the eye, as with
retrobulbar hemorrhage. Another sign of retrobulbar hemorrhage is when globe
pushes against the eyelids, creating such pressures that the eyelid is taut and
cannot be pulled away from from the globe. Always inspect lacerations to ensure
they are not full thickness, and r/o possibility of concealed foreign body, even if
globe seems unaffected, foreign bodies penetrating orbit require immediate
opthalmologic examination to determine if globe is open.
• Extraocular muscles: if patient compliant with orders, then perform finger test,
restricted ocular movement may be from high pressure of orbits, from orbital
fractures, or from muscle or nerve injury.
 • Adnexa: Examine lids for lacerations and its thickness. Examine also for
associated corneal or conjunctival lacerations, because they are often a/w open
globe injuries especially if full thickness.
• Cornea, conjunctiva and sclera: Examine any subconjunctival haemorrhage and
its extent, the more extensive they are, the more likely globe is injured, if
conjunctiva is lacerated, sclera may also be lacerated and may indicate open
globe injury. Abrasions, lacerations or ulcers to conjunctiva or cornea can be
confirmed with fluorescein dye test.
• Iris: If pupils round and reactive to light but slightly larger than pupil of
unaffected eye, patient likely has sphincter tear. If pupil is not round then a small
globe injury may likely have occurred, in this pupils is irregular “peaked”
appearance. Iris may be plugging a hole in globe or poking out from sclera or
cornea in direction in which peaked pupil is pointing a location where full
thickness cornea or scleral laceration would be.
• Anterior chamber: If shallow then leakage of aqueous humor due to an open
globe, closely examine for open globe indicating presence of RBCs, blood in
anterior chamber can be of 2 forms, dispersed (produces haziness) or layered into
top/bottom. A hyphema may elevate IOP and indicate significant trauma to globe.
• Lens: May appear yellowish in elderly. Lens is enclosed in clear taut capsule,
which if violated turns lens into white and produces its swelling over time which
can induce significant intraocular pressure and elevate IOP, unless there is
concomitant large globe injury, if O/E violated lens capsule, then globe most
likely open and eye may contain foreign body.
▪ Posterior segment: Traumatic retinal detachments are not treated emergently. Red
reflex to be observed at minimum.
• Specific ocular injuries: following includes, most time sensitive vision threatening injuries.
◦ Orbit fractures and retro-bulbar haemorrhages: Bleeding around muscle cone, may cause
compartment syndrome behind canthal tendons, on obstructing blood supply to globe
and optic nerve. Signs include decreased vision, elevated eye pressure, asymmetrical
proptosis (eye bulge), resistance to retropulsion and tight eyelids around globe (“rock-
hard eye”). Vision loss can occur 1.5hrs after impaired blood supply, so immediate
treatment is imperative, canthotomy alone (i.e cutting dermis only) does not improve
retrobulbar compartment syndrome, it is cantholysis that increases the size of orbital
compartment, which is equivalent to a fasciotomy. Canthotomy and cantholysis should
not be delayed by obtaining a CT for further evidence.
Orbital fractures and entrap extraocular muscle within fracture site and repair within
48hrs is recommended to avoid muscle ischemia and permanent damage, it is less
common with larger fractures with significant displacment. Larger fractures are more
likely in adults and entrapment with small fractures are more likely in children due to
less brittle bones.
◦ Chemical burns: Ocular emergency, must be treated ASAP, initial treatment involves
copious irrigation of affected eye using a litre of normal saline or ringer’s lactate
connected to a morgan’s lens, lens is placed in eye and head is tilted so that fluid runs
towards temple, if morgan lens unavailable then cut an IV tubing bluntly to maximize
flow. Find out which chemical was involved , was it acid or base, solid or liquid
material. Alkaline compund require more time and more flushing. Powders stick to
superior and inferior fornices of eye and require lid inversion and direct flush with a
syringe to dislodge a granule, after each litre of solution or about every 30 minutes wait
5-10 minutes and check pH of tears, continue cycles of irrigation till pH of 7.0 or
neutral.
◦ Open globes: Occurs with full thickness scleral or corneal penetration, can vary from
microscopic size or gross with visible foreign body. Signs of open globe include peaked
 pupils, shallow AC, abnormal pigmented tissue pushing through sclera or cornea and the
presence of many floating WBCs or RBCs.
Confirmed with siedel test, in an anaesthetized eye a wet fluorescein strip is placed over
the area of concern, while keeping patient from blinking, undiluted fluorescein appears
dark orange in normal light whereas it appears light orange or green under blue light.
Management requires immediate opthalmologic consult and preparation for surgery,
while awaiting further measures can be taken like:
1. Cover the affected eye with a rigid shield and place a paper cup or foam to
accommodate the foreign body, pressure dressing, gauze or other soft material shouldn’t
be placed under the shield as pressure may force further contents out of eye,
furthermore, gauze or soft eye pads can stick to extruding iris or other ocular contents,
which might then be pulled out of eye when removing pad.
2. Provide IV antibiotics, fluoroquinolones like gatifloxacin or levofloxacin are
preferred due to higher concentration in vitreous.
3. Eye moments should be reduced to a minimum, extraocular muscle movement can
extrude intraocular contents, because eye movements are linked to a brain moving good
eye also cause injured eye movement.
4. Treat pain, nausea and coughing. Valsalva manoeuvrers can increase pressure on back
of eye (through venous system), so reduce these activities to help keep intraocular
contents inside eye. If patient is on mechanical ventilation minimize PEEP or coughing.
5. Minimize manipulation of eye. Do not perform any examination beyond visual acuity
and observation.
6. Non contrast CT for fine cuts in orbit (generally 1mm or less) to look for foreign
bodies or other ocular injuries.
Hypothermia and Heat injuries
• Systemic hypothermia:
◦ Defined as core body temperature below 35 C (95F),
◦ Mild (35-32C/95-89.6F), Moderate (32-30C/89.6-86F) or severe (below 30C or 86F)
◦ Concomitant traumatic injury is troubling, and synergy can lead to organ failure and
mortality, hence threshold is different and higher compared to no trauma, i.e mild is
<36C/96.8F, moderate is 36-32C/96.8F-89.6F and severe <32C/89.6F.
◦ Hypothermia also classified based on onset, which can be acute, subacute or subchronic.
▪ Acute hypothermia: Occurs with rapid, sudden cold exposure, as in immersion
within cold water or avalanche, the rapid exposure to low temperatures overwhelms
body’s capacity to maintain normothermia, even when heat production is maximal,
hypothermia takes bout 30 minutes to establish.
▪ Subacute hypothermia: Occurs with depletion of body’s energy reserves,
accompanied with hypovolemia, and treatment involves administration of IV fluids
along with rewarming of patient’s body.
▪ Subchronic hypothermia: Occurs with prolonged exposure to slight cold and
inadequate regulatory system to counter it, classic example is when elderly falls,
sustains hip fracture and lies on ground.
◦ Cold and wet environments provide the greatest risk, disasters and wars are common
settings for hypothermia, but also happens in urban setting with the homeless, in a/w
drug or alcohol use and when fit, young individuals participate in outdoor activities or
work. Elderly more susceptible due to impaired ability to produce heat and decrease heat
loss by vasoconstriction. Children are more susceptible due to increased body surface
area and limited energy sources
◦ Clinical signs:
▪ Shivering in mild hypothermic, skin cool to touch because of vasoconstriction
 ▪ Mental confusion, amnesia, apathy, slurred speech, and loss of fine motor skills in
moderate hypothermia.
▪ Fixed or dilated pupil, bradycardia, hypotension, pulmonary edema, apnea or cardiac
arrest in severe hypothermia.
▪ Respiratory or cardiac activity may be absent or uncommon in individuals who
eventually recover
◦ Cardiac effect: Cardiac output falls in proportion to degree of hypothermia, and cardiac
irritability begins at approximately 33C. ECG findings are nonspecific and includes J
(osborn waves) which is upward deflection at J point after QRS. Ventricular fibrillation
common after temperature falls below 28 C and Asystole may occur when temperature
falls below 25C. Cardiac drugs and defibrillation doesn’t work in presence of acidosis,
hypoxia and hypothermia and such treatments postponed till patient is warmed atleast to
28C.

◦ Management:
▪ ABCDEs:
• Airway management: Same as other cases
• Circulation:
◦ Cardiac arrest: hypothermics frequently land in this, initiate CPR ASAP, and
rewarming. Adrenaline and defibrillation doesnt work until core temperature
rises to 28 C/82.4F. Large bore IV lines or central lines are preferred. IF
subclavian or IJV lines used then the lines are not passed into the heart.
◦ Hypovolemia: A frequent cause of hypothermia, should be corrected with
libberal sue of crystalloid IV fluids
• Breathing: administer 100% O2 as hypothermic patients also have hypoxia which
itself is frequent cause of arrest.
▪ Management according to severeity
Stage/Severity Signs Temperature Treatment
1 (mild) Conscious shivering 35-32C (95-89.6F) • Passive rewarming:
◦ Drying patient,
◦ Covering warm
blankets,
◦ Ingesting warm fluids,
◦ Active movement
(shivering/ambulation),
◦ Cover head.
• Active rewarming
2(moderate) Impaired consciousness, 32-28C(89.6-82.4F) • Immobilization and
not shivering horizontal positioning
• Cardiac monitoring and
minimal cautious
movement to prevent
arrhythmias
• Full body insulation
• Active External rewarming

3(severe) Unconscious, not 28-24C(82.4-75.2F) • Stage 2 management

shivering • Airway management with
either ECMO or with
cardiopulmonary bypass
(CBP only if suspected
cardiac instability
refractory to Tt)
4 (in extremis) No vitals <24 C(<75.2F) • Stage 2 & 3 Management +
CPR + 2-3 dosage of
epinephrine + defibrillation
• Rewarming with ECMO or
CPB or CPR with active
internal and alternative
rewarming.
▪ Active rewarming: Can be external, internal or extracorporeal
• External:
◦ Heating pad
◦ Warm blanket, Warm water ingestion and warm water bottles kept under
blankets
◦ Warm water immersion
◦ External convection heaters (lamps and radiant warmers)
• Internal:
◦ heated IV fluids
◦ Gastric or colonic lavage
◦ Peritoneal lavage
◦ Mediastinal lavage
◦ Warmed inhaled air or oxygen
• Extracorporeal rewarming:
◦ hemodialysis
◦ Continuos arteriovenous rewarming
◦ Continuos venovenous rewarming
◦ Cardiopulmonary bypass
 ▪ Identify and manage comorbid conditions: especially, diabetes, alcohol/drug
ingestion or sepsis. Obtain CBC, LFT,RFT, blood cultures, coagulation profile. Treat
hypoglycemia promptly with IV glucose
▪ Death determination in hypothermia is very difficult and should delay in
announcement till full effort of rewarming has not been performed even if patient
suffered arrest. “you are not dead until you are warm and dead”. Except if
Hypothermia is associated with:
• Anoxic event when patient was in normothermia
• Fatal injury e.g transcerebral gunshot wound, complete exsanguination etc.
• Serum potassium >10mmol/l
• Heat injuries
◦ Heat exhaustion: Caused by excessive loss of body water, electrolytes or both.
Nonspecific symptoms like headache, dizziness, nausea, vomiting, light headedness,
myalagia and malaise. Unlike heat stroke, intact mental function and core temperature
<39C/102.2F. Can potentially worsen into heat stroke.
◦ Heat stroke: Life threatening systemic condition that includes:
▪ Elevated core temperature >40C/104F
▪ Involvement of central nervous system: dizziness, aggressiveness, confusion,
irritability, apathy, disorientation, seizures and coma.
▪ Systemic inflammatory response that includes, acute kidney failure, rhabdomyolysis,
hepatocellular necrosis, myocardial injury, encephalopathy, intestinal ischemia or
infarction, hemaologic condition like DIC and thrombocytopenia.
▪ 2 forms of heat stroke: Classic or non exertional heat stroke occurs due to
environmental heat waves, individuals are elderly or children, children frequently
left alone in vehicles parked in sun.
Exertional heat stroke occurs in healthy, young adults engaged in strenous excercise
or work, in hot and humid environment, it happens due to inadequacy of body’s
regulatory system to handle increase in core body temperature.
▪ Clinical signs: Tachycardia and tachypnea, hypo/normotensive, wide pulse pressure,
skin usually warm or dry or clammy and diaphoretic. Liver and muscle enzymes
elevated in all case
▪ Increased risk in dehydrated, low physical fitness, obese, sleep deprived and
inadequately acclimated individuals
◦ Management:
▪ ABCDEs: Pulmonary aspiration aand hypoxia are most important cause of mortality
• Airway: Adequate airway protection. Patients with altered consciousness,
significant hypercapnia and persistent hypoxia should be intubated and
mechanically ventilated
• Breathing: Administer 100% oxygenation
• Circulation: liberal fluids
▪ Hypokalemia, acidosis and hypoglycemia: Standard treatment. Hypokalemia
develops with acidosis treatment.
▪ Seizures treated with benzodiazepines
▪ Rapid cooling within 30 minutes to decrease core temperature <39C:
• Young, healthy, well trained military personnel or athletes: Iced water immersion
is preferred. Not to be used in elderly
• Elderly: Water spray and airflow, in which er is sprayed at 15C/59F and
circulating warm air that reaches skin at 30-35C(86-95F), effective in unconsious
and hemodynamically unstable patients.
Alternatively Ice packs can be applied at high blood flow regions like groin,
axilla or neck, wet gauze sheet, fans or othe cooling device alone or in
combination can be used.
 • Mass casualty : Specialized body cooling units (BCU)
▪ Medications predisposing to heat stroke should be stopped which include:
• alcohol
• Diuretic
• ACEI
• Antihistaminics
• Anticholinergics
• Caffeine or energy drinks
• Amphetamines or salicylate can increase hypothalamic temperature set point
• Antipsychotic and antidepressants like lithium and SSRI
▪ Factors predisposing to poor prognosis include hypotension, requiring intubation,
altered coagulation, old age, temperature >41c/105.8, long duration of hyperthermia,
prolonged coma, hyperkalaemia and oliguric renal failure.
Bites and Stings
• Snake bite
◦ Venomous snake characteristics:
▪ Crotalinae species: Consist of rattlesnake, copperheads and cotton mouth.
Characteristic features are triangular head, elliptical eyes, Heat sensing facial pits,
large retractable anterior fangs. Hereas nonvenomous noncrtalinae species have
rounded head, circular pupils and no fangs.
▪ Elapidae species: Only non crotalinae species that are venomous, commonly known
as coral snakes. Distinct striped pattern on skin “red on yellow, kill a fellow; red on
black, venom lack”.
◦ Pathophysiology: Crotalinae envenomations consists of 95% cases of snake
envenomations, venom is hemotoxic composed of zinc metalloproteinase disrupting
endothelial basement membrane which can have local effect if deposited in
subcutaneous or intramuscular or can have systemic effect if deposited IV.
Envenomation leads to diffused capillary leakage leading to pulmonary edema,
hypotension and shock, consumptive coagulopathy may follow within 1 hour, organ
dysfunction with shock can happen within minutes. Severity depends on volume of
toxins and its concentration, rattlesnake poisoning is more severe and more likely to
require antitoxin.

Elapidae venom is neurotoxic affecting pre and postsynaptic receptors, producing

respiratory depression progressing to neurogenic shock, they have high risk of mortality
and require immediate medical attention.
◦ Clinical presentation:
 ▪ Crotalinae toxin:
Local effects: Swelling, pain and ecchymosis. Swelling progresses to bullae typically
along the path to lymphatic drainage. Pain starts as burning within minutes of
envenomation, swelling if progressive can develop into compartment syndrome.
Tissue necrosis with further delays.
Systemic effects: From diffuse circulatory collapse, initially nausea, perioral
paresthesia, metallic taste and muscle twitching. Vitals may be tachycardic,
bradycardic or hypotensive
Labs: elevated PT and PTT, fibrin split products, elevated creatinine and creatine
phosphokinase, proteinuria, hematuria and anemia.
▪ Elapidae toxin: Minimal local findings (because of small fang size), Importantly
respiratory depression and neurologic symptoms. Initially nausea, vomiting,
headache, paresthesia or numbness and altered mental status. Neurologic
manifestation Initially starts as cranial nerve dysfunction (e.g ptosis, difficulty
swallowing) f/b peripheral motor weakness and loss of DTRs which may progress to
respiratory depression due to diaphragmatic paralysis and quadriparesis over hours.
Death result from respiratory failure or aspiration.
▪ Sea snake: variable local pain, myalgia, trismus, rhabdomyolysis, and progressive
flaccid paralysis. Delayed for hours.
▪ Palpation of lymph nodes can tell if lymphatic spread of venom has occurred.
◦ Management:
▪ Remove victim from area of danger
▪ Removal of tight fitting clothes or jewellery to prevent constriction and exaggerating
local swelling: be prepared for dysrhythmias or hypotension because of systemic
release of acidotic blood.
▪ Wound to be cleaned locally with running water and soap and covered with sterile
dressing thereafter.
▪ Affected area to be elevated to level of heart.
▪ Applying splint to limit mobility
▪ Elapid venom which is primarily neurotoxic and has minimum local effect may be
managed with pressure immobilization, in which entire bitten limb is wrapped with
bandage and immobilized, it restricts lymphatic drainage and delays neurotoxic
absorption from neurotoxic species.
▪ Patient should not be allowed to walk as muscle pump activity regardless of bite site
disperses venom in systemic circulation.
▪ ABCDEs: bites to face or neck should involve early intubation, Patient bitten by an
elapid should be monitored for ptosis that preceds impending airway compromise, 2
large bore IV lines for Fluid resuscitation with Crystalloids, vasopressors if
refractory to fluids.
▪ Any patients with signs of envenomation should be observed for 24 hours, patients
with even dry bites dry bites should be closely monitored for atleast 8-12 hrs before
discharge, as sisgnificant toxicity may develop after delay of several hours. Those
who have no signs or lab abnormalities can be discharged within 6-8 hours, potential
coral snake envenomation to be observed for longer time, typically 24 hours.
▪ Area of bite should be marked, and the affected area should be assessed every 15
minutes for progression till area stabilized.
▪ CBC to determine degree of hemolysis and thrombocytopenia, blood typing and
cross matching to arrange for PRBC, coagulation studies, D-dimer, RFT, LFT,
creatine kianse for rhabdomyolysis, Thromboelastography for coagulopathies.
▪ Chest x-ray and ECG for older patients or those with systemic symptoms.
▪ CroFab antivenin given depending on severity of crotalinae bites which is
determined using the snakebite severity grading scale. For mild cases CroFab not
 given as its expensive and with its own side effects its only given for moderate and
severe cases.
• Snake bite severity grading scale:
◦ None- fang marks only “dry bite”.
◦ Mild (only from snake saliva and not by venom)- Local findings only (e.g
pain, ecchymosis, nonprogressive swelling)
◦ Moderate-
▪ Local effect: Progressive swelling, swelling that has crossed joint,
swelling involving more than one half of bitten limb, rapidly spreading,
extensive blistering or bruising, severe pain.
▪ Systemic symptoms or signs: Nausea, vomiting, abdominal colic,
confusion, hypotension, tachycardia, metallic taste, perioral paresthesia
and muscle twitching etc.
▪ laboratory abnormalities.
◦ Severe- Neurologic dysfunction, respiratory distress and/or cardiovascular
instability or shock.
◦ Antivenom does not reverse necrotizing tissue damage, it only prevents
further tissue damange and systemic effects
• Antivenom administration after elapid bites are indicated at 1st sign of
neurotoxicity (cranial nerve dysfunction, peripheral neuropathy)
▪ Antivenom may cause acute adverse reaction, so should be administered by IV
slowly, and be in watch for any signs of adverse reaction, if none then the rate can be
increased, till full dose administered. Further antivenom if the clinical condition
worsens or fails to stabilize or venom effects recur. In a stabilized patient further
antivenom administration continues till patient has definite improvement (e.g
reduced pain, stabilized vital signs, restored coagulation).
Neurotoxicity from elapid bites is more difficult to reverse with antivenom. Once
neurotoxicity and ET intubation is required, further dosage are unlikely to be
beneficial. They must remain on ventilation until recovery which may take weeks to
days. Acetylcholinesterase inhibitors may provide improvement, patients with
objective evidence of neurotoxicity should get test dose and if any improvement,
additional doses of long-acting neostigmine can be administered as needed. It should
always be pretreated with atropine to prevent Acetylcholinesterase inhibitor toxicity.
▪ Adverse effects of antivenom includes:
• Early: Anaphylaxis, tachycardia, rigors, urticaria, dyspnea, vomiting, laryngeal
edema, bronchospasm and hypotension. It is managed with IM epinephrine, IV
antihistamines (e.g diphenhydramine) and IV glucocorticoid, once the reaction is
controlled, severity of envenomation warrants additional antivenom at slower
rates. In rare cases of refractory hypotension, a concomitant IV infusion of
epinephrine may be initiatedwhile antivenom is administered.
Such acute adverse reaction may be prevented by with modest expansion of
intravascular volume or with low dose SC epinephrine.
• Late: hypersensitivity reactions like serum sickness that develops 1-2 weeks after
antivenom administration and may present as myalgia, arthralgia, fever, chills,
urticaria, lymphadenopathy, or renal and neurological dysfunction. Treatment for
serum sickness consists of systemic glucocorticoids till all symptoms resolved,
with subsequent taper over 1-2 weeks. Oral antihistamines and analgesia may
provide additional relief of symptoms.
▪ Envenomation may cause decrease platelets, coagulation factors and haematocrit that
usually reverses with antivenom but may require blood products which should be
administered only after adequate administration of antivenom.
 ▪ Rhabdomyolysis if develops should get standard treatment with IV fluids and close
monitoring of urine output, victims who develops acute renal failure should receive
hemodialysis and peritoneal dialysis.
▪ Snake envenomation intramuscularly develops compartment syndrome, for which
intramuscular pressure should be measured, if its high >30-40mmhg then the limb
should be elevated while antivenom is being administered, if intra compartmental
pressure remains elevated after 1 h of treatment, a surgical consult for fasciotomy
should be taken.
▪ Tetanus should be administered.
▪ Antibiotics should be administered only if prehospital measures like incision or
mouth suctioning was done.
▪ Wound care should involve aseptic debridement of clearly necrotic tissue once
coagulopathy has been fully reversed, intact serum filled vesicles or haemorrhagic
blebs should be left undisturbed, if ruptured they should be debrided with sterile
technique.
▪ For patients with progressive clinical findings despite inital antivenom
administration, those bitten in head or neck or other high risk areas and those who
develop hypersensitivity reaction to antivenom.
▪ Antivenom coagulopathy, may recur during the 1st 2-3 weeks after bite as venom
antigens may have longer half lives than the corresponding antivenoms, victims
should be advised to avoid elective surgeries or activities posing high risk of trauma
during this period. Repeat lab tests for coagulopathy to be done.
• Mammalian bites
◦ Most are caused by dogs>cats>humans.
◦ Children more likely to die due to getting bit on face, head and neck.
◦ Injuries can be blunt, penetrating or produce fractures.
◦ Standard wound care with cleaning, debridement and closure.
▪ Primary closure for head and neck wound
▪ Wounds seen longer than 24 hours after bite are covered with moist dressings and
undergo delayed primary closure 3-5 days later
▪ Puncture wound have increased incidence of infection and not sutured. Irrigation and
debridement for large punctures.
▪ Hand and feet bite more likely to be infected and managed with secondary closure
and empiric antibiotics.
▪ Clenched fist injury occurs from human bite due to striking the tooth of another
person, damages the joint capsule and extensor tendon and leads to significant oral
bacterial contamination. Evaluation involves both hand in open and clenched state.
Minor injuries are irrigated, debrided and left open. Potentially deeper injuries and
infection requires exploration and debridement in operating room and administering
IV antibiotics. It is re-evaluated 1-2 days later for secondary infection.
◦ Infections: Caused by staph, strep, Eikinella corroidens (In humans), Pasturella
Multiocida (in Cats>dogs).
▪ Amoxyclav for most bites as 1st line
▪ Infections caused within 24 hours are caused by pasturella
▪ Alternatives include cephalosporin, such as cefoxitin, or a combination of penicillin
and 1st gen cephalosporin
▪ Penicillin allergics may get clindamycin combined with TMP-SMX
▪ Serious infection require Piperacillin-tazobactam, ampicillin sulbactam, and
ticarcillin.
• Arthropod stings
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◦ Black widow: Shiny black body with ventral red hourglass marking.coomon in summer
and early autumn (june to september)
▪ Neurotoxin that releases neurotransmitters like acetylcholine, norepinephrine that
result in excess sympathetic and parasympahtetic activity
▪ Minimal local findings, no pain, only systemic complaints (nausea, vomiting,
cofusion, metallic taste, perioral paresthesia etc.) neuromuscular symptoms only 30
minutes after bite, and include severe painful spasm of large muscle groups of
extremities and trunk. Abdominal cramps and rigidity may mimic surgical abdomen,
but without rebound or tenderness, dyspnea from chest wall muscle tightness. Pain
may resolve within 12 hours but may recur during several days or weeks before
resolving spontaneously. Autonomic hyperactivity results in hypertension,
tachycardia and diaphoresis, other symptoms may include headache, muscle twitch,
hyperreflexia, urinary retention, urine contractions, and premature labor.
Co-morbidities like rhabdomyolysis and renal failure and mortality from respiratory
arrest, cerebral hemorrhage, or cardiac failure.
▪ Treatment:
• Mild bites: Cleansing, intermittent ice and tetanus
• Observation for several hours due to delayed symptoms. Apply RICE
• Severe: narcotics and benzodiazepines to relieve muscles spasm, pain and
hypertension. Hypertension that does not respond to analgesics and
antispasmodics requires specific antihypertensives.
• clinical improvement only with antivenom, although itself can cause anaphylaxis
and serum sickness. Skin allergy testing for antivenom is recommended though
not reliable and patients to be pretreated with IV antihistamines before
antivenom.
◦ Brown recluse spider: Varying degrees of brownish gray, with a characteristic dark
brown, violin shaped marking on top of its head, hence also called violin spider. It also
only has 3 pairs of eyes instead of charcteristic 4.
▪ Generally dwell beneath rocks and logs or in caves and animal burrows. Invade
home and seek dark and undisturbed hiding spots like in closets, garages, crawl
spaces and attics, under furnitures and rubbish in storage rooms and in folds of
clothing. Bites tend to occur when person is donning the cloth in which spider has
hidden itself and sustains primarily on hands, arms, neck and lower abdomen
▪ Major toxin is sphingomyelinase D that causes dermonecrosis and hemolysis, which
is a form of phospholipase that interacts of cell membrane of RBCs, platelets and
endothelial cells which at end result in coagulopathy.
▪ Clinical manifestation:
• Local effect: Bites only cause minor injury with edema and erythema, person
may feel sting or be completely unaware, envenomation may cause severe
necrosis of skin and subcutaneous tissues with ulceration, which is difficult to
differentiate from similar lesions of other arthropods, skin infections (including
MRSA), herpes zoster, dermatologic manifestation of a systemic illness or other
cause of dermatitis and vasculitis.
Within several hours of envenomation pain, itching, swelling and erythema
develops from local tissue Ischemia, a blister may also form at site, in more
severe envenomation the central area may turn purple from microvascular
thrombosis, peripheral vasconstriction can also create a pale border surrounding
the central region, itself surrounded by erythema. In most cases the lesion
resolves on its own within few days, in severe cases the erythema spreads, and
center of lesion becomes hemorrhagic or necrotic with an overlying bulla, which
 over next several weeks develops into a black eschar over the widening necrotic
area, which separates and leaves an ulcer that heals over a period of many weeks
to months (<3 months), leaving behind a depressed scar, but occasionally a skin
grafting is required for treatment. Necrosis is most severe in fatty areas like
abdomen and thigh. Local complications may include injury to nerves or
secondary infection.
• Systemic effects: Fever, chills, headache, nausea, vomiting, malaise, myalgia,
arthralgias and morbilliform rash and leukocytosis over <72 hours. Lab findings
may include thrombocytopenia, DIC, hemolytic anemia and coma and possibly
death. Intravascular hemolysis can result in renal failure.
• In children systemic findings are more predominant with minimal local findings.
▪ Evaluation: CBC and bedside urine test is imprtant 1st tests and if any of these
abnormal follow up with electrolytes, LFT and coagulation studies
▪ Management:
• RICER on bite site: Cold therapy inhibits venom activity. Avodi heat as it
enhances tissue damage and ulceration.
• Tetanus immunization
• Antibiotics: lipophillic prophylactic antibiotics like cephalexin or erythromycin
• Bites without necrosis within 72 hours heals wells with mininmal intervention.
• Antihistaminics like diphenhydramine can be used
• Surgical: Early on only conservative debridement, more extensive intervention to
be avoided as margins of necrosis is unknown and difficult to predict and any
intervention may result in pyoderma gangrenosum of non healing ulcer and in
surgical graft from rapid spread of venom. After 1-2 weeks when eschar margins
are defined debridement can be performed, in severe cases wide excision and
split thickess skin graft may be done.
◦ Scorpion: nocturnal, remain hidden in day, may hide in shoes, bedding or clothes.
▪ Venom is a neurotoxin that maintains sodium channels in open state. Venom also
causes massive release of multiple neurotransmitters hroughout autonomic nervous
system and adrenal medulla
▪ Clinical: minimal local effect but prominent pain, paresthesia and hyperesthesia can
be accentuated by tapping on the affected are (the tap test), this spreads to other
locations, dysfunction of cranial nerves and hyper-excitability of skeletal muscles
develop within hours. Patients present with restlessness, blurred vision, abnormal
eye movements, profuse salivation, lacrimation, rhinorrhea, slurred speech, difficulty
handling secretions, diaphoresis, nausea and vomiting. Muscle twitching, jerking and
shaking may be mistaken for seizures. Complications may include tachycardia,
arrythmia, hypertension, hyperthermia, rhabdomyolysis and acidosis, symptoms
progress to maximal severity within 5 hours and subside within a day or two,
although pain and paresthesia may last for weeks. Fatal respiratory arrest is common
in children and elderly.
▪ Management:
• Nonlethal stings managed with rest, icing, analgesics and antihistaminics.
Compression and icing reduces venom potency
• Requires urgent care if cranial nerve dysfunction or neuromuscular dysfunction
occurs.
• Continuous IV midazolam to control agitation, flailing and involuntary muscle
movement. Narcotics and other sedatives may also be used with close monitoring
for respiratory failure.
• Hypertension and pulmonary edema respond to nifedpine, nitroprusside,
hydralazine or prazosin
• bradydysrhythmia is managed with atropine
 • Scorpion Fab antivenom
◦ Tick bite: 2 types of ticks, hard an soft. Soft ticks do not remain attached for long and
falls off within 1 h, hard ticks remain attached for days to weeks and transmit zoonotic
infections, toxin mediated diseases and autoimmune conditions. Most common species
of hard ticks are ixodes ticks.
▪ Clinical: Feed painlessly, salivary secretions lead to local reactions (swelling,
erythema, itching etc.), induce fevers and cause paralysis.
• Local effects: At site of hard tick bite small areas of induration often purpuric
develop and may be surrounded by an erythematous rim. A necrotic eschar called
tache noire (“black spot”) occasionally develop. If tick bite was persistent then
chronic nodules several centimeters in diameter which are actually granulomas
develop that may linger for months after tick have been removed.
• Systemic: Tick induced fever develops associated with headache, nausea and
malaise, that ususally resolves <36hrs after tick has been removed.
• Paralysis: Ticks saliva may cause ascending flaccid paralysis similar to guillian
barre syndrome, thought to be due to decreased neuromuscular transmission and
decrease nerve conduction. Weakness begins symmetrically in lower extremities
within <6days of tick attachment, ascends symmetrically over several days and
culminate in complete paralysis of all extremities and cranial nerves. DTRs are
diminished or absent, however sensory examination and LP is normal. Dx
depends on finding the tick typically hidden in scalp hair. Failing to remove tick
leads to dysarthria, dysphagia and death from aspiration or respiratory paralysis.
• Autoimmune: Salivary antigens of some ticks particularly lone star tick,
amblyomma americana may induce antibodies to galactose-α-1,3-galactose
(alpha-gal) resulting in mammalian meat allergy-alpha-gal syndrome in which
patient experiences anaphylactic reaction after eating mammalian meat.
• Infections: Tick can transmit illnesses like lyme disease, ehrlichosis, babesiosis
and anaplasmosis
▪ Management:
• Tick is removed by traction with fine tipped forceps placed firmly around tick’s
mouthparts located as close to the patient’s skin, alternatively a suture can be tied
around the mouth part instead of forceps and the tick is pulled gently outward
and backward.
• Tick removal within 36h prevents transmission of zoonotic infection.
• Tick shouldn’t be crushed
• Tick mouthparts may remain embedded but are generally shed within days
without need for surgical removal.
• Removal of ticks also resolves paralysis within days
• Lyme disease prophylaxis is indicated in endemic areas only and within 72 hours
of tick removal. A single dose of oral doxycycline 200mg is given.
◦ Hymenoptera stings:
▪ Management: Site of sting should be cleaned and disinfected and ice packs applied
to slow venom activity. Analgesia, antihistaminincs and topical calamine lotion for
relief of symptoms. Subcutaneous epinephrine for any anaphylactic reaction. Patients
with h/o anaphylaxis should carry anaphylactic kit. Prophylactic immunotherapy to
decrease risk for future reactions.