Pyelonephric Abscess - Structured Examination Answers

a) Pathophysiology and Common Risk Factors of Pyelonephric Abscess (3 Marks)

Pathophysiology

• Extension from adjacent infected structures (Crohn's disease, bowel perforation, spinal osteomyelitis, infected pancreatic pseudocyst)
• Secondary infection of a pre-existing perirenal haematoma

Common Risk Factors

b) Surgical Management - Indications and Methods of Drainage (4 Marks)

General Principles

1. Prompt diagnosis (CT is the gold standard)
2. Early IV antimicrobial therapy
3. Abscess drainage (therapeutic and diagnostic - culture of pus guides antimicrobial choice)

Indications for Drainage

Methods of Drainage

• Performed by interventional radiology under CT or ultrasound guidance
• CT is preferred over ultrasound because it: (a) better characterises abscess extent, (b) maps the spread to psoas/flank/adrenal, and (c) guides needle trajectory
• Technique: image-guided needle aspiration followed by catheter insertion (pigtail drain) into the abscess cavity
• Drain left in place until output ceases and imaging confirms resolution
• Advantages: minimally invasive, can be performed in high-risk/unstable patients, preserves renal function
• Limitation: loculated or multiloculated abscesses may not drain adequately via a single catheter

• Indicated when percutaneous drainage fails, is technically not feasible, or when the abscess is loculated/complex
• Approach: flank incision (retroperitoneal approach), allowing direct exposure of Gerota's fascia
• The abscess cavity is opened, pus evacuated, cavity thoroughly irrigated
• Drains are placed and left in situ post-operatively
• The retroperitoneal approach avoids peritoneal contamination
• Concurrent nephrectomy is performed if the ipsilateral kidney is non-functional or severely pyonephrotic
• In unstable patients, abscess drainage is done first; nephrectomy deferred until the patient stabilises

• Required in ~33% of cases with large abscesses (>11 cm) or non-functioning kidneys
• Indicated when kidney is irreversibly destroyed (pyonephrosis, end-stage infection)
• May be performed laparoscopically if conditions permit

• When abscess results from obstructed ureter (e.g., calculus), ureteral stenting or percutaneous nephrostomy relieves obstruction and allows infected urine to drain
• May be the primary intervention for pyonephrosis with early perinephric extension

c) Postoperative Care and Complications (3 Marks)

Postoperative Care

• Continue IV antibiotics tailored to culture and sensitivity results from abscess fluid, blood, and urine cultures
• Gram-negative cover (aminoglycoside + beta-lactam) is the empiric backbone; add antistaphylococcal cover if haematogenous spread suspected
• Transition to oral antibiotics once the patient is clinically stable and tolerating oral intake
• Total duration: usually 4-6 weeks depending on abscess size and response; continue until imaging confirms complete resolution or stable scar

• Monitor drain output for volume, character, and microbiology
• Serial imaging (ultrasound or CT) to confirm progressive resolution
• Remove drain only when output is minimal and imaging shows collapse of abscess cavity

• Urolithiasis: urological follow-up for stone removal/lithotripsy
• Obstruction: stent/nephrostomy management
• Diabetes: optimise glycaemic control
• Vesicoureteral reflux: urological referral

• Fluid resuscitation and haemodynamic monitoring (sepsis protocol)
• Nutritional support (especially in diabetics or debilitated patients)
• VTE prophylaxis
• Monitor renal function (creatinine, electrolytes)

Complications

• The classic triad is fever + flank pain + failure to respond to antibiotics for pyelonephritis within 4-5 days
• CT abdomen with contrast is the diagnostic gold standard
• E. coli is the most common organism (ascending route); S. aureus suggests haematogenous spread
• Percutaneous drainage is now first-line over open surgery for most abscesses
• Antibiotics alone can suffice only for abscesses < 3 cm in immunocompetent patients
• Always treat the underlying cause (obstruction, calculus, diabetes) to prevent recurrence

Traumatic Brain Injury (TBI) - Structured Examination Answers

a) Pathophysiology of Traumatic Brain Injury (3 Marks)

1. Primary Brain Injury

• Direct contact forces (impact, penetrating injury)
• Inertial forces (acceleration-deceleration, rotational)

• Brain lacerations - direct tearing of parenchyma
• Contusions - bruising of brain surface; most common at the frontal and temporal poles where the brain strikes bony protuberances. Classified as coup (same side as impact) or contrecoup (opposite side)
• Intracerebral haematomas (ICH) - shearing/tensile forces tear deep small-calibre arterioles, causing petechial haemorrhages that coalesce; 85% occur in frontal and temporal lobes
• Diffuse axonal injury (DAI) / Traumatic Axonal Injury (TAI) - rotational and shearing forces stretch and disrupt axons throughout the white matter and brainstem; the extent of brainstem involvement determines depth of coma
• Extra-axial haematomas - epidural (usually from middle meningeal artery injury) and subdural (from bridging vein tears)
• Microvascular injury - permanent disruption at the cellular level

2. Secondary Brain Injury

• Hypotension (SBP <90 mmHg): reduces cerebral perfusion pressure (CPP = MAP - ICP); associated with near-doubling of TBI mortality
• Hypoxia (PaO₂ <60 mmHg): may double mortality; causes include airway obstruction, apnoea from brainstem injury, chest wall injury
• Hypercarbia (PaCO₂ >45 mmHg): causes cerebral vasodilatation → increased ICP
• Hypocarbia (PaCO₂ <35 mmHg): cerebral vasoconstriction → reduced CBF
• Hyperpyrexia (>38.5°C): increases cerebral metabolic demand → elevated ICP
• Anaemia (Hct <30%): reduces oxygen delivery to injured brain

b) Assessment of Suspected TBI in the Emergency Department (3 Marks)

GCS Classification of TBI Severity

Step 1: Primary Survey (ABCDE - ATLS Approach)

• Assume C-spine injury in all blunt trauma (up to ~20% of severe TBI have concurrent cervical spine injury)
• Assess airway patency; intubate if GCS ≤8, inability to protect airway, or signs of impending obstruction
• Maintain in-line cervical stabilisation throughout

• SpO₂ monitoring; target normoxia (SpO₂ >95%)
• Assess for chest injury (haemopneumothorax, flail chest) that may worsen hypoxia

• IV access; target SBP ≥90 mmHg (avoid hypotension - nearly doubles TBI mortality)
• Control external haemorrhage; identify occult haemorrhage (polytrauma)

• GCS (E+V+M, total 3-15): document and trend serially
• Pupillary size and reactivity: unilateral fixed dilated pupil = ipsilateral uncal herniation (CN III compression); bilateral fixed dilated pupils = bilateral transtentorial herniation or brainstem injury
• Lateralising signs: asymmetric motor weakness, Babinski sign
• Blood glucose: exclude hypoglycaemia as cause of altered consciousness

• Full exposure, log-roll, head-to-toe secondary survey

Step 2: History

• Mechanism: high-speed MVC, direction of impact, airbag deployment, ejection
• Loss of consciousness: duration; was there a lucid interval? (suggests epidural haematoma)
• Seizure activity at or after scene
• Amnesia: post-traumatic amnesia duration correlates with injury severity
• Progression: worsening/improving GCS since injury
• Medications: anticoagulants, antiplatelet agents (increase risk of intracranial haemorrhage)
• PMH: coagulopathy, alcohol/drug use

Step 3: Physical Examination

• Scalp inspection and palpation for lacerations, step-offs (depressed skull fracture), haematomas
• Basilar skull fracture signs (Box 33.2 in Rosen's): haemotympanum, periauricular ecchymosis (Battle's sign), periorbital ecchymosis (raccoon eyes), CSF otorrhoea/rhinorrhoea

• Detailed mental status: orientation (to person, place, time), confusion, agitation
• Cranial nerve examination: EOMs, facial nerve, corneal reflexes
• Motor: tone, power, symmetry; decorticate posturing (above midbrain) vs. decerebrate posturing (midbrain level)
• Deep tendon reflexes, plantar responses

Step 4: Diagnostic Investigations

• Indicated for all moderate-to-severe TBI (GCS ≤13) without delay
• Identifies: extradural haematoma (biconvex hyperdense), subdural haematoma (crescent-shaped), contusions, ICH, SAH, cerebral oedema, midline shift, skull fractures
• CT scan findings guide need for neurosurgical intervention
• A CT Angiography should be considered if vascular injury suspected (carotid dissection)

• FBC, coagulation screen (PT/APTT/INR), cross-match
• Urea, electrolytes, creatinine (baseline; hyponatraemia worsens cerebral oedema)
• Blood glucose (bedside)
• Blood alcohol level
• ABG (assess oxygenation and CO₂)

c) Emergency Department Management of Moderate to Severe TBI (4 Marks)

1. Airway Management

• GCS ≤8 (unable to protect airway)
• GCS 9-13 with deteriorating trajectory
• Hypoxia unresponsive to supplemental O₂
• Agitation precluding safe imaging
• Impending herniation

• Pre-oxygenate with 100% O₂
• Maintain in-line C-spine immobilisation
• Induction agent: Ketamine (1-2 mg/kg IV) - preferred (maintains CPP; avoids hypotension); alternatively Etomidate (0.3 mg/kg IV) - haemodynamically neutral
• Neuromuscular blockade: Succinylcholine (1-2 mg/kg IV) or Rocuronium (1.2 mg/kg IV)
• Pre-treat with Lidocaine (1.5 mg/kg IV) - may blunt ICP rise during laryngoscopy
• Avoid hypotension during induction (a single episode of SBP <90 mmHg significantly worsens outcome)
• Post-intubation target: SpO₂ >95%, PaO₂ 80-100 mmHg, PaCO₂ 35-40 mmHg (normocapnia)

2. Haemodynamic Resuscitation

• Target SBP ≥90 mmHg (minimum); Brain Trauma Foundation recommends SBP ≥100 mmHg for age 50-69, ≥110 mmHg for age 15-49
• Fluid resuscitation: isotonic crystalloid (normal saline); avoid hypotonic solutions (worsen cerebral oedema)
• CPP target ≥60 mmHg (CPP = MAP - ICP)
• Treat haemorrhagic shock concurrently - address source of blood loss in polytrauma
• Vasopressors (noradrenaline) if hypotension persists after volume replacement

3. ICP Management

• Head of bed elevation 30° (improves venous drainage, reduces ICP) with neutral head position
• Avoid constrictive cervical collars that impede venous return
• Analgesia and sedation to reduce ICP spikes (morphine, propofol infusion post-intubation)
• Prevent hyperthermia (target normothermia); prophylactic hypothermia is NOT recommended

• Mannitol 20%: 0.25-1 g/kg IV bolus; acts as osmotic diuretic - reduces brain water content; also reduces blood viscosity improving microcirculation; monitor serum osmolality (hold if >320 mOsm/L)
• Hypertonic saline (3%): 2-5 mL/kg IV bolus; emerging evidence suggests superior to mannitol for sustained ICP reduction; preferred in hypotensive patients (does not cause diuresis)

• Not for routine use - causes cerebral vasoconstriction → reduces CBF → ischaemia
• Rescue use only for impending herniation: brief hyperventilation to PaCO₂ 30-35 mmHg as a bridge to definitive neurosurgical intervention
• Normalise PaCO₂ as soon as possible

4. Seizure Management

• Prophylactic antiepileptics are recommended to prevent early post-traumatic seizures (within 7 days)
• Phenytoin/Fosphenytoin (loading dose 15-20 mg/kg IV) - traditional first-line
• Levetiracetam (20-60 mg/kg IV, max 4.5 g) - now preferred in many centres; fewer drug interactions, no need for monitoring
• Prophylaxis does NOT prevent late epilepsy (>7 days)
• If active seizures: Benzodiazepines (lorazepam/diazepam) as first-line, followed by levetiracetam or phenytoin

5. Coagulopathy Management

• Reverse anticoagulation urgently in patients with intracranial haemorrhage
• Warfarin: 4-factor PCC (prothrombin complex concentrate) + Vitamin K IV
• NOACs: specific reversal agents (idarucizumab for dabigatran; andexanet alfa for factor Xa inhibitors)
• Tranexamic acid (TXA): 1 g IV over 10 min within 3 hours of injury - reduces TBI-related mortality in patients without major vessel injury (based on CRASH-3 trial)
• Target platelet count >100 x 10⁹/L in TBI with haemorrhage

6. Neurosurgical Consultation and Indications for Surgery

• Epidural haematoma: >30 mL volume, >15 mm thickness, or >5 mm midline shift - evacuation regardless of GCS; also any EDH with GCS deterioration
• Acute subdural haematoma: >10 mm thickness or >5 mm midline shift regardless of GCS; any SDH with GCS decline >2 points, ICP >20 mmHg, or asymmetric pupils
• Depressed skull fracture: open/compound fractures depressed >1 cm (thickness of skull); also if dural penetration
• ICH/contusion: expanding lesion with mass effect, midline shift >5 mm, or clinical deterioration

• Indicated in all patients with GCS ≤8 and abnormal CT head, or normal CT + age >40, unilateral/bilateral posturing, SBP <90 mmHg
• Treat ICP >20 mmHg

7. What to AVOID (Key Pitfalls)

8. Disposition

• Moderate TBI (GCS 9-13): admit for observation; repeat CT in 4-6 hours or if neurological deterioration; neurosurgery involvement
• Severe TBI (GCS ≤8): ICU admission; ICP monitoring; neurosurgical team activation; consider transfer to neurosurgical centre if not available

1. S - Secure airway, maintain SpO₂ >95%, normocapnia
2. T - Target SBP ≥90 mmHg; treat haemorrhage
3. O - Osmotherapy (mannitol/HTS) for raised ICP
4. P - Prevent seizures, pyrexia, hyperglycaemia
5. S - Scan (CT head urgently) + Surgery if indicated
6. I - ICP monitoring in severe TBI
7. N - Neurosurgical consultation early
8. J - Judicious use of rescue hyperventilation only

Rhabdomyolysis - Structured Examination Answers

a) Pathophysiology of AKI Due to Rhabdomyolysis (2 Marks)

1. Direct Tubular Toxicity of Myoglobin

• Free iron (Fe²⁺/Fe³⁺)
• Ferrihaem (Fe-haem complex)
• Globin

2. Tubular Obstruction (Cast Formation)

• Obstruction of tubular flow → back-pressure → reduced GFR
• Tubular dilation and epithelial injury

3. Intrarenal Vasoconstriction and Ischaemia

• Hypovolaemia (fluid shifts into damaged muscle can exceed 15 litres in crush injury) activates the renin-angiotensin-aldosterone system (RAAS)
• Increased vasoconstricting molecules: endothelin-1, vasopressin, thromboxane A2, TNF-alpha
• Reduced vasodilatory prostaglandins and nitric oxide (NO): myoglobin acts as a NO scavenger in the renal microcirculation, eliminating its vasodilatory effect and allowing uninhibited vasoconstriction
• Consequent renal cortical ischaemia → acute tubular necrosis (ATN)

• Acidosis/aciduria (worsens cast formation and tubular toxicity)
• Hyperuricaemia (uric acid crystals obstruct tubules)
• Hypovolaemia (reduces renal perfusion)

b) Clinical Features of Rhabdomyolysis (2 Marks)

Symptoms

Signs

c) Common Causes of Rhabdomyolysis (2 Marks)

Classified by Mechanism (Tintinalli's Table 89-1 / Rosen's Table 116.1)

• Marathon running, military basic training, CrossFit, spinning
• Seizures, delirium tremens, dystonia, psychosis
• Status epilepticus, status asthmaticus
• Sickle cell crisis, alcohol withdrawal

• Crush injury (most classic: seismic disasters, entrapment)
• Motor vehicle accidents
• Prolonged immobilisation (coma, post-operative)
• Electrical/lightning injury
• Burns

• Statins (particularly with polypharmacy: cyclosporin, macrolide antibiotics, gemfibrozil)
• Drugs of abuse: cocaine, amphetamines/ecstasy, heroin, methadone, PCP, LSD
• Ethanol (direct toxicity + coma-induced compression)
• Antipsychotics, benzodiazepines, barbiturates, SSRIs
• Colchicine, corticosteroids, theophylline, succinylcholine

• Viral: influenza A/B, EBV, CMV, HSV, HIV, coxsackievirus, rotavirus, hepatitis
• Bacterial: Legionella, Clostridium, Staphylococcus aureus, Streptococcus pyogenes, Salmonella

• Heatstroke, hyperthermia
• Malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome
• Hypothermia

• Hypokalaemia, hypophosphataemia, hypocalcaemia, hyponatraemia/hypernatraemia

• Dermatomyositis, polymyositis

• Glycolysis/glycogenolysis disorders (McArdle disease)
• Fatty acid oxidation disorders, mitochondrial chain disorders
• G6PD deficiency, muscular dystrophies

• Arterial occlusion (embolus, thrombus), vascular surgery

d) McMahon Score and its Role in Prognosis (2 Marks)

Scoring Parameters (from Tintinalli's Table 89-2)

Score Interpretation

Clinical Role

• Guides triage and disposition: high scores warrant ICU admission, aggressive resuscitation, and early nephrology consultation
• Identifies patients who need intensive monitoring for developing AKI requiring dialysis
• Helps risk-stratify patients for aggressive vs conservative fluid management, especially when resuscitation carries its own risk (e.g., heart failure)
• The score is particularly useful in the ED to determine the threshold for early nephrology referral

e) Emergency Department Approach: Laboratory Tests, Imaging, and Treatment (2 Marks)

Step 1: Initial Stabilisation

• Two large-bore IV cannulas; cardiac monitoring (hyperkalaemia risk)
• Continuous pulse oximetry, O₂ supplementation as needed
• Urinary catheter for strict urine output monitoring (target: 200-300 mL/hour)

Step 2: Key Laboratory Investigations

Step 3: Imaging

• Not routinely required for the diagnosis of rhabdomyolysis itself
• Compartment pressure measurement if compartment syndrome suspected (pain out of proportion, tense compartment, paraesthesias)
• Ultrasound/MRI of muscles if localised infection or abscess is the aetiology
• Renal ultrasound if urinary obstruction is a concern or kidneys cannot be assessed otherwise

Step 4: Treatment

• Normal saline (0.9% NaCl) is the first-line fluid
• Initial bolus: 1-2 litres IV rapidly if hypotensive, then continuous infusion
• Infusion rate: 200-1000 mL/hour titrated to urine output target of 200-300 mL/hour
• Aim to maintain urine pH >6.5 to reduce cast formation and tubular toxicity
• Continue until CK trending down AND urine clears AND haemodynamics stable
• Avoid hypotonic fluids (worsen hyponatraemia)
• Sodium bicarbonate (8.4% NaHCO₃ - 50-100 mEq IV): sometimes added to alkalinise urine (target urine pH >6.5) and correct metabolic acidosis; however, its benefit over normal saline alone is not definitively proven, and use is controversial if the patient is hypocalcaemic (alkalosis worsens hypocalcaemia)
• Mannitol (0.5 g/kg IV): may be added as an osmotic diuretic to increase urine flow and reduce tubular obstruction; also may scavenge free radicals; controversial - should only be considered after adequate volume resuscitation

• Stop offending medications (statins, etc.)
• Treat infection with appropriate antibiotics
• Cooling for hyperthermia/heatstroke
• Anticonvulsants for seizures

• Urgent surgical fasciotomy if compartment pressure >30 mmHg or within 30 mmHg of diastolic BP

1. Refractory metabolic acidosis
2. Life-threatening hyperkalaemia unresponsive to medical therapy
3. Fluid overload with oliguria
4. Manifestations of uraemia

Disposition