Trauma Resuscitation (ATLS), Burns, Hernias & Perioperative/Post-Operative Surgical Care

Tension pneumothorax presents with hypotension, distended neck veins, absent unilateral breath sounds, hyperresonance to percussion, and contralateral tracheal deviation; treat immediately with needle decompression (2nd intercostal space midclavicular line or 5th intercostal space anterior/midaxillary line) followed by tube thoracostomy—never delay for a chest X-ray. Massive hemothorax presents with shock, flat neck veins, dullness to percussion, and absent breath sounds; place a large-bore (28–36 Fr) chest tube, and proceed to urgent exploratory thoracotomy if initial chest tube output exceeds 1,500 mL of blood immediately or continues at >200 mL/hr for 2–4 consecutive hours. Cardiac tamponade presents with Beck's triad (hypotension, jugular venous distension, muffled heart sounds), pulsus paradoxus (>10 mmHg inspiratory drop in systolic BP), and electrical alternans; diagnose via subxiphoid eFAST pericardial window and treat with emergency pericardiocentesis or subxiphoid pericardial window / thoracotomy. Open pneumothorax (≥2/3 tracheal diameter) is treated immediately with a three-sided occlusive dressing (taped on three sides to create a flutter valve preventing tension pneumothorax) followed by chest tube placement at a separate site. Traumatic aortic rupture occurs after high-speed deceleration motor vehicle collisions at the aortic isthmus (just distal to the left subclavian artery at the ligamentum arteriosum), showing a widened mediastinum (>8 cm), apical pleural cap, and left hemothorax on CXR.

Penetrating neck injuries that breach the platysma muscle are stratified into three anatomical zones: Zone I (clavicles/sternal notch to the cricoid cartilage; contains the aortic arch branches, subclavian vessels, trachea, esophagus, thoracic duct, and lung apices), Zone II (cricoid cartilage to the angle of the mandible; contains the common/internal/external carotid arteries, internal jugular veins, larynx, pharynx, and vagus nerve), and Zone III (angle of the mandible to the skull base; contains the distal internal carotid artery, vertebral arteries, and cranial nerves IX–XII). Regardless of zone, any patient presenting with hard signs of vascular or aerodigestive injury (hemodynamic instability, pulsatile bleeding, expanding hematoma, bruit/thrill, loss of carotid pulse, airway compromise, subcutaneous emphysema, or bubbling air from the wound) goes immediately to the operating room for surgical exploration. In hemodynamically stable patients with only soft signs (non-expanding hematoma, minor hemoptysis, dysphonia, dysphagia) or no signs, modern high-resolution CT angiography (CTA) of the neck is the first-line diagnostic modality across all three zones (followed by esophagography/esophagoscopy and bronchoscopy if aerodigestive injury is suspected).

In blunt abdominal trauma: (1) If the patient is hemodynamically unstable (SBP <90 mmHg, HR >120 bpm), perform an immediate bedside eFAST exam (or Diagnostic Peritoneal Lavage [DPL], which is positive if >10 mL gross blood is aspirated or >100,000 RBCs/mm3); a positive eFAST/DPL in an unstable patient mandates immediate exploratory laparotomy. (2) If the patient is hemodynamically stable, obtain a CT scan of the abdomen and pelvis with IV contrast; Grade I–III solid-organ (splenic or hepatic) lacerations in stable patients without active contrast extravasation (“arterial blush”) are managed non-operatively with serial hemoglobin checks and ICU observation (or angioembolization if an arterial blush is present on CT), whereas unstable patients or Grade V shattered/avulsed spleens require splenectomy (followed by mandatory vaccination against encapsulated bacteria: S. pneumoniae, H. influenzae type b, and N. meningitidis 14 days post-splenectomy). In penetrating abdominal trauma: nearly all abdominal gunshot wounds violate the peritoneum and require immediate exploratory laparotomy (except isolated right upper quadrant tangential GSWs in stable patients), whereas anterior abdominal stab wounds in hemodynamically stable patients without peritonitis or evisceration can undergo local wound exploration at the bedside (if anterior rectus fascia is intact, discharge home; if violated, perform serial abdominal exams, CT, or diagnostic laparoscopy). High-speed lap-belt deceleration injuries in children and adults classically cause a duodenal hematoma (bilious vomiting with obstruction; managed conservatively with NGT decompression and TPN for 1–2 weeks), retroperitoneal duodenal perforation, pancreatic transection over the spine, and a lumbar Chance fracture.

High-energy open-book pelvic fractures tear the posterior pelvic venous plexus and internal iliac arterial branches,retroperitoneally accommodating up to 4–5 liters of blood. Immediate bedside management requires wrapping a pelvic binder or sheet centered over the greater trochanters (not the iliac crests!) to tamponade venous bleeding. If the patient remains unstable with a positive FAST, proceed to exploratory laparotomy; if the FAST is negative (indicating retroperitoneal pelvic hemorrhage), proceed to preperitoneal pelvic packing or interventional radiology pelvic angiography with internal iliac embolization. Intraoperatively, retroperitoneal hematomas are divided into three zones: Zone 1 (Central/Medial—aorta, IVC, pancreas, duodenum): always explore for both blunt and penetrating injuries; Zone 2 (Flank/Perirenal—kidneys, renal vessels): explore for penetrating injuries or expanding/pulsatile blunt hematomas; and Zone 3 (Pelvic—iliac vessels): explore for penetrating injuries, but DO NOT open a blunt Zone 3 pelvic hematoma at laparotomy (opening the retroperitoneum releases the tamponade and triggers fatal exsanguination—pack and send to angioembolization). In exsanguinating patients developing the lethal triad (hypothermia <35°C, acidosis pH <7.2, coagulopathy), perform Damage Control Laparotomy: control surgical hemorrhage, staple off hollow-viscus contamination without formal anastomoses, leave a temporary open-abdomen vacuum dressing to prevent abdominal compartment syndrome (bladder pressure >20 mmHg with oliguria and elevated peak airway pressures), resuscitate in the ICU with a 1:1:1 ratio of pRBCs, Fresh Frozen Plasma, and Platelets plus tranexamic acid (TXA within 3 hours), and return for definitive repair in 24–48 hours.

Burns exceeding 15–20% TBSA trigger massive systemic capillary leak during the first 24 hours, requiring intravenous crystalloid resuscitation with Lactated Ringer's calculated via the Parkland Formula: Total 24-Hour Fluid (mL) = 4 mL × Body Weight (kg) × %TBSA (2nd and 3rd degree only). Crucially, one-half (50%) of the total volume is administered over the first 8 hours calculated from the exact time of the burn injury (not from time of ED arrival—so if a patient arrives 2 hours post-burn, the first half must be infused over the remaining 6 hours), and the second half (50%) is infused over the subsequent 16 hours. The Parkland calculation is only a starting point; ongoing infusion rates are titrated strictly to maintain hourly urine output of ≥0.5 mL/kg/hr in adults (30–50 mL/hr) and ≥1.0 mL/kg/hr in children (<30 kg) (or 1.0–1.5 mL/kg/hr in high-voltage electrical burns with rhabdomyolysis/myoglobinuria). A circumferential full-thickness (3rd-degree) burn of an extremity or the thorax creates an unyielding leathery eschar that acts as a tourniquet as resuscitation edema accumulates—causing limb compartment syndrome (loss of distal Doppler pulses, paresthesias) or restrictive chest wall asphyxiation (skyrocketing peak inspiratory pressures and hypercapnia); the immediate bedside treatment is emergency longitudinal escharotomy (incising only through the insensate burn eschar into subcutaneous fat along the medial/lateral limb midlines or anterior axillary lines of the chest).

Patients rescued from enclosed-space house fires presenting with facial burns, singed nasal vibrissae, carbonaceous sputum, hoarseness, stridor, or bronchorrhea require immediate prophylactic endotracheal intubation before progressive supraglottic thermal edema completely occludes the airway, paired with 100% FiO2 for concomitant carbon monoxide poisoning (diagnosed via carboxyhemoglobin on co-oximetry; standard pulse oximetry is falsely normal) and hydroxocobalamin if cyanide toxicity is suspected (profound lactic acidosis >10 mmol/L). In deep burns, Succinylcholine is strictly contraindicated after 24–48 hours post-burn because upregulation of extrajunctional nicotinic acetylcholine receptors across denervated/injured muscle membranes causes massive, fatal hyperkalemic cardiac arrest (use non-depolarizing rocuronium instead). Topical antimicrobial prophylaxis utilizes silver sulfadiazine (causes transient leukopenia; avoid on the face and near the eyes) or mafenide acetate (uniquely penetrates full-thickness eschar and auricular cartilage to prevent suppurative chondritis of the ear, though it inhibits carbonic anhydrase and causes non-anion-gap metabolic acidosis). Invasive burn wound sepsis—marked by rapid separation of eschar, violaceous-black hemorrhagic discoloration (ecthyma gangrenosum), and systemic hypotension—is most commonly caused by Pseudomonas aeruginosa or Staphylococcus aureus.

Step 1: Screen for four active unstable cardiac conditions that mandate delaying elective surgery for immediate cardiology workup/stabilization: (1) unstable coronary syndromes (acute MI within 60 days or unstable angina), (2) decompensated heart failure, (3) significant arrhythmias (high-grade AV block, symptomatic ventricular arrhythmias), and (4) severe valvular disease (symptomatic severe aortic stenosis or mitral stenosis). Step 2: Estimate perioperative risk using the 6-point Revised Cardiac Risk Index (RCRI) (1 point each for: high-risk suprainguinal vascular/intraperitoneal/intrathoracic surgery, history of ischemic heart disease, history of congestive heart failure, history of cerebrovascular disease/stroke/TIA, insulin-dependent diabetes mellitus, and pre-operative serum creatinine >2.0 mg/dL). If RCRI is 0–1 (low risk, <1% MACE), proceed directly to surgery without cardiac testing. If RCRI is ≥2 (elevated risk), assess functional capacity: a patient who can achieve ≥4 METs without cardiopulmonary symptoms (e.g., climbing one flight of stairs, walking up a hill, walking on level ground at 4 mph, or heavy housework) can proceed directly to surgery without stress testing! Pharmacologic stress testing (dobutamine stress echo or nuclear myocardial perfusion) is reserved strictly for patients with elevated risk (RCRI ≥2) AND poor or unknown functional capacity (<4 METs) in whom test results would change management. After coronary revascularization, elective non-cardiac surgery must be delayed at least 14 days after balloon angioplasty, 30 days after a bare-metal stent (BMS), and 6 months after a drug-eluting stent (DES) to prevent fatal perioperative stent thrombosis upon stopping P2Y12 inhibitors.

Managing chronic medications on the morning of surgery is heavily tested on COMAT and Step 2/3 exams: CONTINUE chronic beta-blockers (withdrawal causes rebound tachycardia/MI; however, never initiate a high-dose beta-blocker de novo on the morning of surgery due to increased stroke/hypotension mortality), statins, clonidine, inhaled bronchodilators, levothyroxine, and anti-epileptics. HOLD on the morning of surgery: ACE inhibitors and ARBs (cause refractory intraoperative hypotension after anesthesia induction), oral hypoglycemics (metformin held 24–48 hr to prevent lactic acidosis; SGLT2 inhibitors held 3–4 days to prevent euglycemic DKA; sulfonylureas held to prevent hypoglycemia), and diuretics. For insulin: hold short-acting prandial insulin while NPO, and administer 50–80% of the usual long-acting basal glargine/detemir dose (or 50% NPH) with a dextrose-containing IV infusion (target perioperative blood glucose 140–180 mg/dL). Patients taking chronic systemic corticosteroids (≥20 mg/day prednisone equivalent for >3 weeks within the past year) have HPA-axis suppression and require stress-dose IV hydrocortisone prior to moderate/major surgery to prevent acute adrenal crisis. For anticoagulants/antiplatelets: hold warfarin 5 days pre-op (target INR <1.5; bridge with LMWH only for mechanical mitral valves or high-risk VTE, holding the last therapeutic enoxaparin dose 24 hours pre-op), hold DOACs (apixaban, rivaroxaban, dabigatran) 48–72 hours pre-op, hold clopidogrel 5–7 days, hold NSAIDs 3–7 days, and hold aspirin 7 days (EXCEPT continue aspirin in patients with coronary stents or undergoing carotid endarterectomy/CABG). Intraoperatively, Malignant Hyperthermia (autosomal dominant RYR1 ryanodine receptor defect triggered by volatile inhaled anesthetics [sevoflurane, isoflurane, desflurane] or depolarizing succinylcholine) presents with an abrupt rise in end-tidal CO2 (the earliest sign), masseter spasm, generalized muscular rigidity, tachycardia, rhabdomyolysis, hyperkalemia, and extreme hyperthermia (a late sign); immediately stop the triggering agent, hyperventilate with 100% O2, and administer intravenous dantrolene (contrasted with anesthesia-induced postoperative nausea/vomiting, treated with ondansetron).

POD 1–2 (Wind / Necrotizing Infection): Most early fevers stem from surgical cytokine release (IL-1, IL-6, TNF-alpha) and pulmonary atelectasis (managed with incentive spirometry, early ambulation, deep breathing, and osteopathic rib raising). However, a high fever on POD 1–2 accompanied by severe wound pain, crepitus, or thin dishwater-gray/salmon-colored drainage indicates fulminant necrotizing surgical site infection caused by Clostridium perfringens or Group A Streptococcus pyogenes, requiring immediate surgical debridement plus IV penicillin and clindamycin. POD 3–5 (Water): Urinary tract infection (CAUTI from indwelling Foley catheter; confirm with urinalysis/culture and remove catheter). POD 4–6 (Walk): Deep vein thrombosis or pulmonary embolism (pleuritic chest pain, abrupt hypoxia, sinus tachycardia; confirm with CT pulmonary angiography). POD 5–7 (Wound / Anastomotic Leak): Typical Staphylococcus aureus surgical site infection presents with erythema, warmth, induration, and purulent drainage (open staples/sutures, drain, and pack; add antibiotics if cellulitis exceeds 2 cm or systemic SIRS is present), whereas an anastomotic leak after bowel resection or Roux-en-Y gastric bypass presents on POD 5–7 with fever, unexplained persistent tachycardia, leukocytosis, abdominal pain/peritonitis, or bilious/feculent drainage (confirm with water-soluble contrast CT or upper GI series; unstable/generalized peritonitis requires immediate re-exploration and washout/diversion, whereas a contained small abscess <3 cm takes IV antibiotics and ≥3 cm undergoes CT-guided percutaneous drainage). Sudden gush of large-volume salmon-colored (serosanguinous) fluid from an abdominal incision on POD 5–8 after coughing/straining signals fascial dehiscence (separation of the linea alba/rectus fascia): if skin remains intact and bowel does not protrude, manage conservatively with an abdominal binder; if bowel protrudes through the wound (evisceration), cover the bowel immediately with warm sterile saline-soaked gauze and proceed to the operating room for emergency fascial closure.

Post-operative paralytic ileus is a functional, non-mechanical inhibition of gastrointestinal motility after abdominal surgery mediated by splanchnic sympathetic hyperactivity (T5–L2), peritoneal inflammation, opioid analgesia, and electrolyte derangements (hypokalemia and hypomagnesemia). Patients present with abdominal distension, nausea, intolerance of oral intake, absent/hypoactive bowel sounds, and diffuse dilation of both the small and large intestines with gas in the rectum on abdominal radiographs; management is supportive (NPO, IV fluids, electrolyte repletion, minimizing opioids via multimodal ketorolac/epidural analgesia, early ambulation; routine NGT placement is needed only for refractory vomiting). Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome) occurs in elderly, hospitalized, or post-orthopedic/cardiothoracic surgery patients and presents with massive dilation isolated to the cecum and right/transverse colon without a mechanical transition point on CT/water-soluble enema. Because Laplace's law dictates that wall tension is highest in the wide-diameter cecum, a cecal diameter >12 cm carries an imminent risk of ischemic cecal perforation; first-line treatment (after ruling out mechanical obstruction and stopping opioids/anticholinergics) is supportive care for 24–48 hours, followed by intravenous neostigmine (an acetylcholinesterase inhibitor that restores parasympathetic vagal/pelvic splanchnic colonic motility; monitor on cardiac telemetry with atropine at the bedside for severe bradycardia) or colonoscopic decompression.

The boundaries of Hesselbach's triangle are: Medial = lateral border of the rectus abdominis muscle, Lateral = inferior epigastric vessels, and Inferior = inguinal (Poupart) ligament. (1) An Indirect inguinal hernia is the most common hernia overall in both men and women (and children); it arises from congenital failure of the processus vaginalis to obliterate, entering the deep (internal) inguinal ring LATERAL to the inferior epigastric vessels, traversing the entire inguinal canal within the spermatic cord (covered by all 3 spermatic fascial layers: external, cremasteric, and internal), and exiting the superficial (external) ring into the scrotum or labium majus. (2) A Direct inguinal hernia arises from acquired weakness of the transversalis fascia (floor of the inguinal canal) in older men due to chronic intra-abdominal pressure (COPD, BPH, heavy lifting, constipation); it protrudes directly through Hesselbach's triangle MEDIAL to the inferior epigastric vessels, covered only by external spermatic fascia, rarely enters the scrotum, and has a low risk of strangulation because of its wide neck. (3) A Femoral hernia protrudes inferior to the inguinal ligament through the femoral ring into the femoral canal, located medial to the femoral vein and lateral to the lacunar ligament (remembered by NAVEL from lateral to medial: femoral Nerve, Artery, Vein, Empty space [femoral canal hernia site], Lymphatics/Lacunar ligament). Although less common than indirect inguinal hernias, femoral hernias occur much more frequently in females (due to a wider female pelvis) and carry the highest rate of incarceration and strangulation of all groin hernias because of the rigid boundaries of the femoral ring.

Surgical boards frequently test five classic named hernias: (1) Obturator hernia (“little old lady's hernia”): occurs in thin, elderly, multiparous women due to loss of pelvic floor fat, where bowel herniates through the obturator canal alongside the obturator nerve, presenting with small bowel obstruction and a positive Howship-Romberg sign (lancinating pain radiating down the medial thigh to the knee exacerbated by hip extension, abduction, and internal rotation); (2) Richter hernia: entrapment and strangulation of only the antimesenteric wall of the small intestine within a tight hernia ring—causing ischemia, necrosis, and perforation without causing luminal bowel obstruction (patients continue to pass flatus/stool until perforation occurs); (3) Littre hernia: any hernia sac containing a Meckel diverticulum; (4) Spigelian hernia: ventral herniation through the semilunar line along the lateral border of the rectus sheath at the arcuate line (diagnosed via ultrasound or CT because it remains interparietal beneath the external oblique aponeurosis); and (5) Sliding vs. Pantaloon hernia: a sliding hernia has a retroperitoneal viscus (sigmoid colon or urinary bladder) forming part of the wall of the hernia sac itself, whereas a Pantaloon (saddlebag) hernia combines concurrent ipsilateral direct and indirect inguinal sacs straddling the inferior epigastric vessels. In infants, congenital umbilical hernias close spontaneously and are observed until age 4–5 years (unless incarcerated or >2 cm), whereas pediatric indirect inguinal hernias never close spontaneously and require prompt elective high ligation of the hernia sac (herniotomy) due to high incarceration risk.