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• Boxer's fracture Fracture of the fifth metacarpal neck. Due to forward trauma of a closed fist (eg, punching a wall) Treatment: Closed reduction and ulnar gutter splint; percutanous pinning if the fracture is excessively angulated.
• Hip fracture Classified according to their anatomical location as intracapsular (femoral head and neck) and extracapsular (intertrochanteric, trochanteric, and subtrochanteric) - ↑ risk with osteoporosis - Presents with a shortened and externally rotated leg- Can be radiographically occult, so good clinical history with ⊝ radiographs warrants further evaluation with CT or MRI.- Displaced femoral neck fractures associated with ↑ risk of avascular necrosis and nonunion. Complications: Avascular necrosis of the femoral head (especially femoral neck fractures), DVTs Femoral head fracture: Pipkin Classification  Treatment:- Femoral head: Prosthesis- Intertrochanteric: Plates- Shaft: Rod- Anticoagulate to ↓ the likelihood of DVTs.
• Anterior cruciate ligament tear Higher incidence in females Mechanism of injury:- Low-energy noncontact: sports injuries with a twisting mechanism, e.g., football, soccer, basketball, baseball, alpine skiing, and gymnastics - High-velocity contact injuries (less common): direct blows to the knee causing forced hyperextension or valgus deformity of the knee Clinical features:- Audible pop followed by knee swelling (e.g., hemarthrosis), pain, and instability- Positive Lachman test (most sensitive test)- Positive anterior drawer test- Positive pivot shift test- Features of other ligamentous or meniscal injuries: The unhappy triad includes tears of the anterior cruciate ligament, medial collateral ligament, and the medial meniscus (i.e., tender joint line, poor knee extension) Diagnosis:- Joint aspiration (in the case of severe joint effusion): hemarthrosis- MRI (confirmatory test) Treatment:- Conservative treatment for mild knee instability, less physically demanding occupations, or premorbid inactivity→ RICE protocol (rest, ice, compression, and elevation of the affected limb)→ Analgesia→ Physical therapy- Arthroscopic surgery for multiligament injuries, chronic knee instability, and for highly competitive athletes 
• Posterior cruciate ligmanet tear Mechanism of injury:- Noncontact injury involving hyperflexion of the knee with a plantarflexed foot (seen in athletes) - Direct posterior blow to a flexed knee, seen in motor vehicle accidents (dashboard injury) or athletic contact injury Clinical features:- Initially vague symptoms: minimal (or absent) posterior knee pain, swelling, functional range of motion- Positive posterior drawer test- Positive posterior sag sign- Positive quadriceps active test- Positive posterolateral drawer test Diagnosis:- X-rays initially: avulsion fracture, posterior sag of the tibia- MRI (confirmatory test) Treatment:- Conservative therapy for isolated injuries- Surgery for multiligament injuries, chronic knee instability, and for highly competitive athletes
• Collateral ligament injury Medial collateral ligament injury- Most commonly injured knee ligament- Mechanism of injury: valgus stress with possible external rotation- Clinical features→ Knee swelling with ecchymosis (e.g., hemarthrosis), pain, deformity, and instability→ Medial joint line tenderness→ Valgus stress test: Medial joint laxity→ Frequently associated with medial meniscal tear Lateral collateral ligament injury- Isolated LCL injury is very rare; it is usually associated with a tear of the anterior and/or posterior cruciate ligaments, as well as the posterolateral corner (PLC)- Mechanism of injury: varus stress with possible external rotation - Clinical features→ Knee swelling with ecchymosis, pain, deformity, and instability→ Lateral joint line tenderness→ Varus stress test: Lateral joint laxity Diagnosis: An isolated tear is a clinical diagnosis, but x-rays and MRI can be used to assess for associated injuries. Treatment:- Conservative treatment (including a functional brace) for isolated tears- Surgery if multiligament injury is present
• Meniscus tear Etiology:- Twisting injuries of the knee- Minimal trauma in older patients due to chronic degeneration of the cartilage Clinical feature:- Knee pain: exacerbated by weight‑bearing or physical activity- Joint line tenderness (medial or lateral)- Restricted knee extension with knee instability→ Locked knee may occur if the torn meniscus obstructs knee movement.→ May hear clicking sound or have a popping or locking sensation- Intermittent joint effusions (see dancing patella sign)- Effusions develop slowly and may not be apparent until the next day Signs:- Tenderness at the joint line- Thessaly test: Patient stands on 1 leg with knee flexed 20°. Patient then internally and externally rotates on flexed knee.- McMurray test: The examiner flexes the knee to 45°. The examiner holds the medial side knee in one hand and ankle in the other hand. The examiner then externally rotates the leg and brings the knee into extension.- Steinman test: The examiner fixes the bent knee with one hand. The examiner grasps the foot with their other hand and rotates the tibial head internally and externally.- Apley grind test: Similar to the Steinman test but performed in a prone position- Payr test: The patient sits cross-legged. The examiner applies pressure from above on both knees simultaneously. Diagnosis: MRI
• Stress fracture Risk factors:- Repetitive activities (eg, running, gymnastics)- Abrupt increase in physical activity- Inadequate calcium & vitamin D intake- Decreased caloric intake- Female athlete triad: low caloric intake, hypomenorrhea/amenorrhea, low bone density Clinical features:- Insidious onset of localized pain- Point tenderness at fracture site- Possible negative x-ray in the first 6 weeks Diagnostics:- X-ray is normal for 2 weeks Management:- Reduced weight bearing for 4-6 weeks- Cast and crutches
• Ottawa rules X-ray of the ankle is required if:- Pain at the malleolar zone AND- Tender at posterior margin/tip of medial malleolus OR- Tender at posterior margin/tip of lateral malleolus OR- Unable to wear weight 4 steps X-ray of the foot is required if:- Pain at the midfoot zone AND- Tender at the navicular OR- Tender at the base of the 5th metatarsal OR- Unable to bear weight 4 steps 
• Achilles tendon rupture Risk factors: Pre-existing degenerative conditions (including polyarthritis), ↓ poor physical condition, medication (glucocorticoids, chinolones, immunosuppressants). Presentation:- Popping or snapping sound/sensation- Loss of plantar flexion power on the affected side - Calf swelling (ie, hematoma) and/or palpable interruption of the affected Achille's tendon- ⊕ Thompson test: squeezing the calf (ie, gastrocnemius muscle) in prone position with legs extended leads to absent passive plantar flexion. Diagnostics:- Clinical- Ultrasound, X-ray (rule out avulsion fracture), MRI (distinguish between partial and complete rupture) Treatment: Surgery followed by a long-leg cast for 6 weeks.
• Compartment syndrome ↑ pressure within a muscle compartment (containing nerves and vasculature, enclosed by unyielding fascia) leads to impaired tissue perfusion. Etiology:- External compressing forces: Burn eschars, constrictive bandage/cast- Internal compressing forces: Fracture hematoma, blood vessel injury with hemorrhage, crush injury, penetrating injuries (e.g., gunshot and stab wounds), burn edema, reperfusion syndrome with ischemia-reperfusion edema Symptoms:- Pain out of proportion to physical findings- Pain with passive stretching or extension of muscles- 6 P's: Paresthesia, pallor, poikilothermia, pulselessness, paralysis Subtypes:- Anterior compartment syndrome of the lower leg (most common)- Abdominal compartment syndrome Diagnosis:- Compartment pressures (initial and confirmatory test): measurement of tissue pressure with a manometer and calculation of delta pressures (diastolic - tissue pressure). Delta pressure in manifest compartment syndrome: ≤ 30 mm Hg- Laboratory tests specific for rhabdomyolysis Treament: Immediate fasciotomy  Differential: Deep vein thrombosis, acute limb ischemia, rhabdomyolysis
• Basilar skull fracture Clinical features:- Liquorrhea: leakage of CSF from the subarachnoid space through an external opening→ Due to a dural tear immediately or within the first few days after the trauma→ May show a halo sign: rapidly-expanding clear ring of fluid surrounding blood- Subcutaneous hematoma- Cranial nerve palsies: usually arise 1-3 days after the trauma Anterior basilar skull fracture- CSF rhinorrhea: leakage of CSF from the nose- Subcutaneous hematoma around the eyes (“raccoon eyes”)- Can cause cranial nerve I, V, VI, VII, or VIII palsies Posterior basilar skull fracture:- CSF otorrhea: leakage of CSF from the external auditory meatus- Hemotympanum- Subcutaneous hematoma behind the ear (Battle sign)- Can cause cranial nerve VI, VII, or VIII palsies; in rare cases, causes facial numbness by damaging CN V Diagnostics: CT head and neck
• Neck trauma - Hard/soft signs Airway:- Gurgling- Stridor- ApneaSoft signs: Dysphonia, subcutaneous air Vessels:- Expanding hematoma- Pulsating bleeding- Frank shock- StrokeSoft signs: Hematoma, oozing Digestive:- Frank mediastinitisSoft signs: Dysphagia, subcutaneous air
• Neck trauma Unstable (hard signs) → ALL go to surgery Stable:- Upper zone (III) → Arteriogram (carotid artery)- Middle zone (II) → Safely explored (easy access)- Basal zone (I) → Esophagram, bronchogram, arteriogram (jugular, carotid, esophagus, trachea)
• Hemothorax Etiology:- Penetrating or blunt trauma- Nontraumatic: malignancy, pulmonary embolism with infarction, TB, giant bullous emphysema Clinical features:- Dyspnea and diminished/absent breath sounds- Decreased tactile fremitus, dullness on percussion- Chest pain- Flat neck veins, hemorrhagic shock and respiratory distress in severe hemorrhage Diagnostics:- Chest x-ray: similar appearance to pleural effusion: Opacity, blunting of the costophrenic angle, tracheal deviation (mediastinal shift)- Ultrasound: detection of smaller amounts of fluid/blood than on chest x-ray possible Treatment:- Chest tube insertion into the 6th or 7th intercostal space at the posterior axillary line- Thoracotomy indicated if→ Chest tube output > 1000 mL immediately after placement or 150-200 mL/hour for 2-4 hours→ Multiple transfusions required Complications: pleural empyema; fibrothorax and trapped lung
• Pulmonary contusion Clinical features:- Present < 24 hours after blunt thoracic trauma- Tachypnea, tachycardia, hypoxia- Chest pain Diagnosis:- Rales or decreased breath sounds- X-ray: patchy alveolar infiltrates; diffuse opacity or 'white out'- CT scan (most sensitive)  Treatment:- Pain control- Pulmonary hygiene (eg, nebulizer treatment, chest PT)- Supplemental oxygen & ventilatory support- Avoid crystalloids (ringer lactate and normal saline) and fill the vascular volume with colloids (blood and albumin)- Diuretics and PEEP Complications- Pneumonia- ARDS
• Cardiac injury Myocardial contusion: - Cardiac arrhythmia (palpitations, dizziness, syncope)- Hypotension and tachycardia that do not respond to fluid resuscitation Myocardial rupture: - Hypotension, muffled heart sounds- Most patients die before reaching the hospital. Diagnostics:- Best initial test: ultrasound (FAST)- Serial ECGs and echocardiography Treatment:- Cardiac monitoring- Cardiac rupture: immediate surgery
• Blunt abdominal trauma - Most common: liver injury > splenic injury (e.g., hematoma, laceration) - Severe bleeding- Pancreatic contusion, laceration, or rupture (through direct epigastric impact, e.g., handlebar injury)- Diaphragmatic rupture- Traumatic injuries of the kidney and bladder- Duodenal damage and hematoma: common injury in children who suffer blunt abdominal trauma- Pelvic fracture- Abdominal compartment syndrome Clinical features:- Pain, tenderness- Abdominal distention; guarding or rigidity- Signs of abdominal bleeding: hemodynamic instability/shock (hypotension, tachycardia, cyanosis), anxiety, flank discoloration- If liver hematoma: Ecchymoses over the right chest + referred pain in the right shoulder (due to diaphragmatic irritation) Approach:- Unstable → FAST → Fluid → Laparotomy- Stable → CT scan  Conservative treatment:- Angiography and embolization (e.g., control bleeds, manage low retroperitoneal hematomas)- Management of pancreas injury: percutaneous drainage (with culture) and debridement to prevent complications (pseudocysts, abscess)- Management of duodenal injury: nasogastric suction and parenteral nutrition to allow healing; if patients remain unstable, laparotomy may be indicated.
• Snake bites Most venomous snake bites occur in developing countries. Venomous snakes:- Slit-like eyes- Rattlers- Cobra cowl Effects of venom:- Bleeding due to coagulopathy- Increase in capillary permeability, which leads to:→ Local edema→ Accumulation of interstitial fluid in the lungs- Neuromuscular blockade- Cardiac failure can result from hypotension and acidosis Treatment:- Anti-venom IV- ø torniquet/cut/suck
• Black widow bites Black spider with an hourglass on the belly (highly unlikely to see it and get bit) Clinical features:- Abdominal pain or pancreatitis- Muscle pain, muscle cramps (> 60% of patients)- Nausea and vomiting Treatment: IV calcium gluconate to stabilize muscles
• Brown recluse spider bite Found in attic or old boxes (especially in the south) Occur as patients are putting their clothes on Clinical features:- Day 1: Asymptomatic- Day 2: Small ulcer → Necrotic ulcer with ring of erythema Treatment:- Wide debridement- Skin graft
• Isopropyl Found in Rubbing alcohol Effects: isopropyl alcohol is metabolized to acetone → ↑ serum ketones Clinical features:- Altered mental status, coma- Nausea, vomiting, abdominal cramps- Fruity mouth odor- Massive ingestion: features of shock Diagnostics:- ↑ Osmolar gap (not in alcohol) Treatment: Supportive
• Methanol Sources of exposure:- Fuels (highly flammable)- Ingested as ethanol substitute by alcoholics- Self-harm attempts- Improper distillation of spirits; comes from moonshine Effects: Metabolism of methanol in the liver → accumulation of formic acid and formaldehyde in the blood → anion gap metabolic acidosis (seen on blood gas analysis) → severe nerve damage Maximum effect: 48 hours after intoxication Clinical features:- Nausea, abdominal cramps- Headache, altered mental status- Severe acidosis- Optic neuropathy associated with vision problems and blindness Diagnostics:- Anion gap acidosis- ↑ Osmolar gap Treatment: Fomepizole
• Carbon monoxide poisoning Exposure: house fires, wood-burning stoves, motor vehicle exhaust, furnaces in enclosed and poorly ventilated spaces Properties: Colorless, odorless, and tasteless gasAffinity to hemoglobin ∼ 240 times stronger than that of oxygen → formation of COHb (carboxyhemoglobin) Pathophysiology: ↑ COHb causes tissue hypoxia by the following mechanisms:→ Decreased oxygen carrying capacity of hemoglobin→ Shift in the O2 dissociation curve to the left → decreased release of O2 in tissues→ Binding of CO to myoglobin → cardiac ischemia → decreased cardiac output→ CO inhibits mitochondrial cytochrome c oxidase → defective oxidative phosphorylation → decreased ATP production Clinical features:- COHb levels 10-30%: fatigue, headache, nausea- COHb levels > 30%: agitation, confusion, memory loss, somnolence, dyspnea, chest pain- COHb levels > 50%: shock, respiratory failure, myocardial infarction, seizures, coma- Postmortem findings: light red livor mortis (“cherry-red” skin tone), salmon-colored muscles- Inhalational injury in the event of fire burns Diagnosis: - High anion-gap metabolic acidosis - Cranial CT: bilateral hypodensity of globus pallidus- ECG: arrhythmias, evidence of myocardial ischemia- Chronic CO poisoning: ↑ hemoglobin- Normal SpO2 on pulse oximetry- Confirmatory test: ↑ COHb in arterial or venous blood Treatment:- Patients with inhalation injury: intubation- 100% oxygen via non-rebreather facemask, until asymptomatic and COHb levels normalize- Hyperbaric oxygen therapy is indicated if: COHb > 25%; Pregnant women with a COHb > 15%; Neurological manifestations; Acute myocardial ischemia; Severe acidosis (pH < 7.1)
• Cyanide poisoning Examples: CN-, HCN , KCN Exposure:- Fires: Cyanide is released by various substances during combustion (e.g., plastics, upholstery, rubber). - Long-term or high-dose treatment with sodium nitroprusside, especially in patients with chronic renal failure- Industrial: metal industry, manufacture of nitrogen-containing materials and products (plastics and wool), electroplating Pathophysiology: absorbed through the skin, respiratory system, and gastrointestinal tract- Cyanide blocks the electron transport chain by binding to cytochrome complex IV → ↓ oxidative phosphorylation → anaerobic metabolism, ↑ lactic acid Clinical features:- Breath smells of bitter almonds- Neurologic symptoms: confusion, agitation, vertigo, headache, seizures, coma- Gastrointestinal: nausea, vomiting, discomfort- Cardiopulmonary symptoms: dyspnea, chest pain, cardiac arrhythmia, respiratory failure- Bright red bleeding of mucous membranes- Flushing of the skin- Necroses in mouth and esophagus- Bright red retinal veins on fundoscopic examination- Postmortem, bright red livor mortis can be seen- Blood tests: high anion gap metabolic acidosis, ↑ lactic acid Management:- Decontamination of the patient (e.g., remove clothes, wash skin)- Administration of 100% oxygen, supportive care- Antidote:→ Hydroxycobalamin (precursor of vitamin B12): binds cyanide directly and forms cyanocobalamin, which is excreted in urine.→ IV sodium nitrite, amyl nitrite, or 4-dimethylaminophenol (4-DMAP): induce methemoglobinemia; methemoglobin binds to cyanide to form cyanomethemoglobin, which diverts cyanide from cytochrome complex IV and increases oxidative phosphorylation.→ IV sodium thiosulfate: supplies sulfur donors to the mitochondrial enzyme rhodanese, which detoxifies cyanide into thiocyanate, which is excreted in urine. Consider cyanide poisoning in a patient with chronic renal failure who has very recently undergone treatment for a hypertensive emergency and is now presenting with altered mental status and lactic acidosis!
• Organophosphate poisoning Examples: parathion (E605), fungicides, insecticides, herbicides, malaria control agents, nerve gases, pharmaceutical drugs (e.g., pyridostigmine, donepezil) Pathophysiology: Absorbed through the skin, respiratory system, or gastrointestinal tract- Irreversible inhibition of acetylcholinesterase → ↑ acetylcholine levels → activation of muscarinic and nicotinic acetylcholine receptorsResult: life-threatening activation of parasympathetic nervous system Clinical features: cholinergic crisis:- Garlic or petrol-like odor- Blue-colored saliva and mucosa- Cardiovascular symptoms: bradycardia, hypotension- Gastrointestinal symptoms: ↑ salivation, diarrhea, abdominal pain, uncontrolled urination- Bronchospasm- CNS-related symptoms: restlessness, anxiety, ataxia, tremor possibly culminating in coma- Musculoskeletal symptoms: fasciculations, weakness, spasms, paralysis → peripheral neuromuscular respiratory failure- Ocular symptoms: miosis, lacrimation Management:- Decontamination of the patient (e.g., remove clothes, wash skin)- Secure airways, ECG- Measurement of erythrocyte cholinesterase activity: ↓ acetylcholinesterase activity- Medication→ Atropine → Pralidoxime, obidoxime: Should only be administered after atropine due to risk of transient worsening of acetylcholinesterase inhibition The greatest danger in organophosphate poisoning is respiratory failure!
• Salicylate poisoning More common in children (accidental overdose) Clinical features:- Early symptoms: tinnitus, nausea, vomiting, tachypnea, hyperpnea- Severe toxicity: hyperthermia, agitation, delirium, seizures, noncardiogenic pulmonary edema Diagnosis:- ABG analysis: mixed respiratory alkalosis; increased anion gap metabolic acidosis- Serum salicylate levels- Renal function tests and electrolyte levels: ↑ BUN and creatinine and/or hypokalemia Treatment:- Stabilization of vitals- Oral/orogastric activated charcoal: indicated if time since ingestion is < 3 hours- IV sodium bicarbonate- Hemodialysis
• Clavicle fracture Clinical features:- Tenting of skin overlying the clavicle- Shortening of the clavicle Diagnostics:- Assess for neurovascular compromise and compartment syndrome→ Weak pulses: possible injury of the subclavian artery→ Dysfunction of a distal nerve: possible injury of the brachial plexus- X-ray in two projections Treatment:- Midshaft: conservative (e.g., simple shoulder sling) for 4-6 weeks- Lateral: Stable → conservative; unstable → surgical fixation- Medial: conservative
• Splenic abscess Risk factors:- Infection (e.g., infective endocarditis) with hematogenous spread- Hemoglobinopathy (e.g., sickle cell disease)- Immunosuppression (e.g., HIV)- IV drug use- Trauma Clinical presentation:- Classic triad of fever, leukocytosis & left upper-quadrant abdominal pain- Left-sided pleuritic chest pain with left pleural effusion- Possible splenomegaly- Most commonly due to Staphylococcus, Streptococcus & Salmonella- Usually diagnosed by abdominal CT scan Treatment:- Combination of broad-spectrum antibiotics & splenectomy- Possible percutaneous drainage in poor surgical candidates
• Prosthetic joint infection Early onset: < 3 months- Acute pain- Wound infection or breakdown- Fever- Pathogens: S. aureus, gram-negative rods, anaerobes Delayed onset: 3-12 months- Chronic joint pain- Implant loosening- Sinus tract formation- Pathogens: Coagulase-negative staphylococci, Propionibacterium, enterococci Late onset: > 12 months- Acute symptoms in previously asymptomatic joint- Recent infection at distant site- Pathogens: S. aureus, gram-negative rods, β-hemolytic streptococci
• Malignant hyperthermia A subclinical myopathy in which general anesthesia triggers an uncontrollable contraction of skeletal muscle that leads to a life-threatening hypercatabolic state and increase in body temperature. Etiology:- Inherited susceptibility: primarily autosomal dominant with reduced penetrance→ ∼ 50% of cases: associated with a mutation in the ryanodine receptortype 1 (RYR-1) .- Volatile anesthetic agents (e.g., sevoflurane, enflurane, halothane, isoflurane, desflurane)- Succinylcholine Clinical features:- Tachycardia- Tachypnea- Cyanosis- Rigidity- Late signs: Elevated body temperature (up to 45ºC/113°F)- Complex arrhythmias- Oliguria (acute kidney injury)- Seizures- Bleeding and/or thrombosis (disseminated intravascular coagulation)- Myoglobinuria, muscle pain, swelling, and weakness of the affected muscles (rhabdomyolysis) Diagnostics:- Respiratory parameters: continuous increase in end-tidal CO2- Arterial blood gas: ↑ pCO2, ↓ pO2, and ↑ lactate: mixed respiratory and metabolic acidosis- Electrolyte abnormalities: hyperkalemia, hypercalcemia- Myoglobinemia, increased creatine kinase Treatment:- Immediate administration of dantrolene (ryanodine receptor antagonist)- Stop administration of potential triggering agents!- Increase respiratory minute volume by at least 3-fold.- Ventilation with 100% O2- Rapid completion of surgery
• High-energy trauma of the lower extremities E.g., calcaneus fracture following a fall from a height → Perform thoracolumbar spine x-rays to look for additional injuries
• Blunt trauma with subcutaneous emphysema Perform bronchoscopy for diagnosis of injury to the trachea and then perform surgical repair.
• No blood in the urinary meatus, but hematuria through Foley catheter Perform retrograde cystogram for diagnosis of bladder injury.
• Blood in the urinary meatus Perform retrograde urethrogram (may be a bladder injury, but need to rule out urethral injury first).
• Large hematoma over the shaft of the penis Perform emergent surgical repair of penile fracture.
• Cushing triad ↑ Intracranial pressure → ↓ perfusion pressure within the brain → compensatory activation of the sympathetic nervous system to maintain cerebral perfusion → ↑ systolic blood pressure → stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia ↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing Triad:1. Hypertension2. Bradycardia3. Irregular respiration
• Splenic rupture Etiology:- Blunt abdominal trauma: Most frequently caused by motor vehicle accidents Clinical features:- Diffuse abdominal pain, especially in the left upper quadrant (LUQ), possible abdominal guarding- Kehr's sign: referred pain in the left shoulder - Ballance's sign: dullness on percussion in the LUQ- Hemorrhagic shock (often delayed): tachycardia and hypotension- In delayed splenic rupture, symptoms may not present until days to weeks after trauma Diagnostics:- Laboratory tests: low Hb, leukocytosis, and thrombocytosis; crossmatch for blood transfusion if needed- In hemodynamically unstable patients→ First ultrasound: focused assessment with sonography (FAST)a) Koller pouch: splenorenal recessb) Morrison's pouch: hepatorenal recessc) Pouch of Douglas: between the rectum and, the bladder (in males) or uterus (in the females)→ If free intraabdominal fluid → diagnostic laparoscopy/laparotomy- In hemodynamically stable patients→ Method of choice: abdominal CT scan (with contrast) Treatment:- If low-grade injury in hemodynamically stable patients → Conservative management (e.g. hospital observation with frequent ultrasound examination)- If high-grade splenic injuries and/or hemodynamically unstable patients → Laparotomy 
• Fat embolism syndrome Potentially life-threatening condition caused by the entry of fat cells, usually form bone marrow, into the circulatory system Etiology:- Traumatic fat embolism (95% of cases)→ Long bone fractures→ Orthopedic surgeries→ Bone marrow transplant- Non-traumatic fat embolism: Sickle cell crisis, pancreatitis, osteomyelitis, parental lipid infusion Clinical features:- Symptoms develop within 12 hours to 2 weeks of the inciting insult- Classic triad of1. Hypoxia: tachypnea, dyspnea, cyanosis, diffuse crackles in the chest2. Neurological symptoms: confusion, lethargy, seizures, focal neurological deficits, coma3. Petechial rash (in 50%): mainly seen in the axilla, chest wall, head, neck, conjunctiva, buccal mucosa Diagnostics:- CBC: anemia, thrombocytopenia- Chest x-ray: mostly normal; bilateral infiltates may be seen- Microscopic examination of urine and sputum: fat droplets may be seen Treatment: supportive Most patients improve with correction of hypoxia (supplemental oxygen or intubation and mechanical ventilation). Vasopressors/IV albumin may be required in hypotensive patients. IV corticosteroids/heparin are controversial treatment options.
• Blunt cardiac injury Rapid deceleration or direct blow to the precordium → shearing, compression, abrupt pressure change Clinical spectrum:- Arrhythmia ranging from asymptomatic (e.g., PVCs) to fatal (e.g., VFib)- Acute coronary syndrome from coronary dissection or thrombosis- Myocardial dysfunction ("myocardial contusion")- Ruptured valve, septum, or ventricular wall- Cardiac tamponade Confirmatory testing:- ECG- Echocardiogram
• Blunt genitourinary trauma Diagnostics:- Urinalysis- Hemodynamically stable with evidence of hematuria → contrast-enhanced CT scan- Hemodynamically unstable with evidence of renal trauma → intravenous pyelography prior to surgical evaluation
• Risk of surgical site infection Patient factors:- Malnutrition/hypoalbuminemia, obesity- Glucocorticoids, immunosuppressive drugs, chemotherapy, radiation- Smoking- Uncontrolled diabetes, peripheral artery disease, venous insufficiency- Concurrent infection at another site- Advanced age Procedural factors:- Emergency surgery- Surgery for malignancy- Open surgical approach- Inadequate site preparation & antibiotic prophylaxis
• Diaphragmatic rupture Etiology: penetrating injuries (65%), blunt trauma (35%) Clinical features:- Often initially asymptomatic- Chest/abdominal wall bruises- In case of herniation of abdominal organs into the chest: Decreased breath sounds, bowel sounds in the thorax, respiratory distress- Signs of bowel obstruction Diagnostics:- Chest x-ray: → Disturbed contour of the hemidiaphragm→ Displaced abdominal organs (esp. stomach and bowel segments): hourglass sign→ Possible mediastinal shift→ Nasogastric tube visible above the left hemidiaphragm- Ultrasound FAST: rapidly detect large tears or herniation- CT scan to confirm the diagnosis Complications: diaphragm paralysis Treatment: most patients require surgery
• Methemoglobinemia Methemoglobin contains iron in its oxidized (ferric = Fe3+) rather than its reduced state (ferrous = Fe2+) and cannot bind oxygen. Methemoglobin levels:0-3% of total hemoglobin: physiological> 3%: visible cyanosis (a brownish-blue or grayish coloration of the skin and membranes)> 20%: clinical symptoms of oxygen deprivation; brown blood ("chocolate-colored blood")> 70%: fatal Causes of methemoglobinemia:- Nitrate or nitrite- Drugs: nitroglycerin, sulfonamides, dapsone, inhaled nitric oxide, topical anesthetics such as lidocaine, and aniline derivatives- Nitro and amino compounds of benzene Diagnosis:- Dark brown coloration of blood- Reduced oxygen saturation and total oxygen content with normal PaO2 on arterial blood gas analysis despite clinical signs of cyanosis- Confirm with CO-oximeter. Treatment:- Methylene blue: At lower concentrations, it is very effective in reducing methemoglobin to hemoglobin. - Reducing agents such as ascorbic acid (vitamin C) and riboflavin may help reduce methemoglobin to hemoglobin, although they are not always effective.- Last resort: exchange transfusion
• Post-transplantation morbidity < 1 month: Bacterial causes from operative complications (e.g., hepatic abscess, biliary leak, wound infection) or hospitalization (e.g., intravascular catheter, external drain) Months 1-6: Opportunistic pathogens (e.g., CMV, Aspergillus, Mycobacterium tuberculosis) in the setting of high-dose immunosuppressive medication > 6 months: Immunosuppressants usually at maintenance levels. Patients primarily at risk for typical community-acquired pathogens (at a higher rate than the general population) Hyperacute reaction: < 1 week after transplantation Acute cellular rejection: < 90 days after transplantation- Fever, right upper quadrant pain, elevated LFT
• Shin splint Medial tibial stress snydrome Epidemiology:- Casual runners- More common in overweight patients (vs. underweight in stress fractures) Clinical features:- Anterior leg pain resembling that of a stress fracture- Diffuse area of tenderness
• Abdominal compartment syndrome Etiology:- Penetrating abdominal trauma- Pelvic trauma- Rupture of abdominal aortic aneurysm- Massive volume resuscitation (e.g., postoperative patients, treatment of hypovolemic shock, severe burns)- Severe ascites- Abdominal surgery- Sepsis Pathophysiology: ↑ intra-abdominal pressure → organ dysfunction Clinical features: may develop within hours or over days- Critically ill patient- Cardiovascular: signs of increased central venous pressure (e.g., distended jugular veins), hypotension, tachycardia- Renal: oliguria, progressive renal failure- Gastrointestinal: tight, distended abdomen, nausea, vomiting- Pulmonary: tachypnea, wheezing Diagnostics:- Best initial test: indirect measurement of intra-abdominal pressure (Can be indirectly measured by measuring the pressure in the bladder via an intravesical catheter)- CT imaging: increased abdominal diameter, compression of the inferior vena cava, intestinal wall thickening, bilateral inguinal herniation Treatment:- Abdominal decompression→ Laparotomy for decompression→ Temporary abdominal closure (e.g., patch technique, vacuum-assisted closure)→ Definitive closure- Supportive management→ Percutaneous drainage of intra-abdominal fluid→ Hemodynamic stabilization (e.g., fluid resuscitation, transfusions)→ Ventilation
• Fascial dehiscence Fascial disruption due to abdominal wall tension that overcomes tissue or suture strength, or knot security Early dehiscence:- Profuse serosanguinous drainage, possible “popping” sensation or bulge during Valsalva maneuvers- 4-14 days after surgery- Surgical emergency → could lead to organ evisceration Late dehiscence:- Incisional hernia Treatment for early dehiscence:- Cover wound with moist dressing → wound exploration and debridement in OR- Can use abdominal binder to keep organs intact while en route to OR- Reapproximate fascial edges- Closure with continuous, slowly absorbable suture Complications:- Organ evisceration: abdominal organs protrude through the outer abdomen→ If evisceration has happened, do not use binder → take to OR immediately Prevention: good surgical technique, avoid heavy lifting for 4-6 weeks after abdominal laparotomy
• Hematomas and seromas Collection of blood (hematoma) or serum (seroma) Risk factors:- Obesity- Hypocoagulability (e.g., anticoagulation, coagulopathy) Clinical features:- Usually occurs several days after surgery- Either asymptomatic or can have swelling, pain, or drainage Treatment:- Small or asymptomatic: manage expectantly- Large or symptomatic: exploration and drainage, followed by wound packing until granulation tissue is formed, then closed by delayed primary intention or by secondary intention Complications: may lead to wound infections as bacteria have access to deeper layers of fascia and can multiply in the stagnant fluid
• Groin hernias Indirect inguinal hernia:- Male infants- Pathophysiology: Patent processus vaginalis- Originates lateral to inferior epigastric vessels- Protrudes through the deep inguinal ring into the inguinal canal- May extend into the scrotum (following spermatic cord) Direct inguinal hernia:- Older men- Pathophysiology: Weakness of the transversalis fascia- Protrudes medial to the inferior epigastric vessels into Hesselbach's triangle- May pass through the superficial inguinal ring- No direct route into the scrotum Femoral hernia:- Women- Pathophysiology: Widening of the femoral ring- Emerges inferior to the inguinal ligament- Protrudes through the femoral ring into the femoral canal

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