---

Anaesthetic Management: SDH with Midline Shift (Conservative Neurosurgical Management) Posted for Bone Fracture Right Leg

---

THE CLINICAL SCENARIO — Framing the Challenge

• An active intracranial pathology (subdural haematoma [SDH] with midline shift, on conservative management — meaning the neurosurgical team has judged it does not yet warrant surgical evacuation)
• An urgent orthopaedic procedure (long-bone fracture of the right leg, likely requiring either regional or general anaesthesia)

---

PART 1 — UNDERSTANDING THE INTRACRANIAL PATHOPHYSIOLOGY

1.1 The Monro-Kellie Doctrine

"When the cranium is closed, the objectives are to maintain adequate CPP (CPP = MAP – ICP) and prevent the herniation of brain tissue between intracranial compartments or through the foramen magnum." — Miller's Anesthesia, 10e (Chapter 53)

1.2 CT Findings Signalling Elevated ICP / Reduced Compliance

• Midline shift ✅ (present in this patient)
• Obliteration of basal cisterns
• Loss of sulci / sulcal effacement
• Ventricular effacement
• Hypodense areas = vasogenic oedema

The basal cisterns appear as a dark (hypodense) halo around the upper brainstem on CT — comprising the interpeduncular cistern, quadrigeminal cistern, and ambient cisterns. Their obliteration signals transtentorial herniation risk.

1.3 Clinical Signs of Raised ICP

1.4 Herniation Pathways (Miller's Fig. 53.1)

---

PART 2 — PREOPERATIVE ASSESSMENT

2.1 Glasgow Coma Scale (GCS) — Mandatory Assessment

• GCS ≤ 8: Airway no longer reliably protected — intubation required
• GCS < 15 after TBI: CT scan is mandatory
• GCS < 15 with any intracranial lesion on CT → consider ICP monitor for surgery within 48 hours

"If there has been a loss of consciousness at any time or if the GCS score is less than 15, a CT scan should be obtained. If the CT reveals compressed basal cisterns, midline shift, or effaced ventricles, an ICP monitor should be considered for surgery with general anesthesia performed within 48 hours after TBI." — Miller's Anesthesia, 10e (Chapter 53, ICP Monitoring for Non-Neurologic Surgery)

2.2 The "Talk and Die" / Delayed Deterioration Phenomenon

"Excessive comfort should not be taken from a good GCS score. Patients with good scores can talk and deteriorate or talk and die after a TBI associated with loss of consciousness. Delayed deterioration has been observed as much as 4 days after the initial injury."

• Frontal and frontotemporal contusions
• Medial temporal lesions (near uncus/incisura — herniation can occur at relatively low ICP ≥20 mmHg)

2.3 World Federation of Neurological Surgeons (WFNS) Scale

2.4 Injury Severity Score (ISS) — For the Combined Trauma Patient

2.5 Three Key Variables for Non-Neurological Surgery Decision (Miller's)

1. Level of consciousness — GCS, CT findings, ICP monitor consideration
2. Time since injury — Delayed deterioration up to 4–4.5 days; if within this window with CT lesion + GCS <15 → ICP monitoring strongly advised
3. Nature and duration of the intended procedure — A 6-hour spine instrumentation in prone position carries far greater ICP risk than a 20-minute wound debridement

---

PART 3 — RECURRENT ISSUES IN NEUROANESTHESIA (Box 53.1, Miller's)

---

PART 4 — ICP TARGETS AND CPP MANAGEMENT

4.1 ICP Threshold

• Normal ICP: 5–15 mmHg
• Treatment threshold: ICP > 22 mmHg (Brain Trauma Foundation guidelines, updated)
• Lethal ICP: Sustained > 40 mmHg

4.2 CPP Targets

"CPP should be kept between 60 and 70 mmHg, as higher or lower values worsen outcome after head trauma."

"A single episode of systolic hypotension below 90 mm Hg may double mortality in patients with severe head injury."

4.3 Dysautoregulation — The Critical Concept

• Autoregulation may be lost → CBF becomes pressure-passive
• Even "normal" MAP can cause ischaemia if resting CBF is already low (as commonly occurs in first 24 hours after injury)
• Implication: Hypotension during anaesthetic induction/maintenance, even to normally acceptable levels, may produce cerebral ischaemia in these patients

---

PART 5 — PREOPERATIVE OPTIMISATION

Checklist Before Taking Patient to OR

• Jugular venous pressure — avoid extreme head rotation, direct jugular compression; ensure head-up 30°
• Airway pressure — airway obstruction? Bronchospasm? Excessive PEEP?
• PaCO₂ and PaO₂ — normocapnia; normoxia
• Arterial pressure — maintain MAP, avoid hypotension

• Pain/arousal — adequate analgesia and sedation
• Seizures — anticonvulsant therapy if indicated
• Fever — normothermia (each 1°C rise increases CMR ~7%)

• N₂O, volatile agents at high concentrations, nitroprusside, calcium channel blockers — all increase CBV/ICP

• Expanding SDH? Intracerebral haematoma? Air + N₂O expansion?

Pre-op Medications to Optimise

---

PART 6 — ICP MONITORING DECISION

Indications for ICP Monitor Before This Surgery

• GCS < 15 after loss of consciousness + CT showing midline shift → strong indication for ICP monitor
• Surgery within 48 hours of TBI with CT lesion
• Lengthy general anaesthesia planned
• Frontal/temporal lesions at risk for delayed herniation

"The ventricular catheter is still the gold standard of measurement as long as the ventricles are accessible, because they reflect global ICP and allow therapeutic drainage of CSF."

---

PART 7 — ANAESTHETIC MANAGEMENT IN THE OPERATING ROOM

7.1 Goals of Anaesthesia

1. Avoid hypotension — CPP = MAP – ICP; hypotension is lethal
2. Avoid hypoxia — SpO₂ must be ≥ 95% continuously
3. Control CO₂ — Normocapnia (PaCO₂ 35–38 mmHg); mild hyperventilation (30–35 mmHg) if ICP rises
4. Avoid ICP surges — Smooth induction, intubation without coughing
5. Euvolaemia with isotonic fluids — No hypotonic solutions; no albumin in TBI

7.2 Premedication

• Anxiolytics with caution — avoid respiratory depression and CO₂ rise
• Aspiration prophylaxis: consider full stomach protocol (trauma patients)
• Continue antiepileptics

7.3 Monitoring

• ECG, SpO₂, NIBP (arterial line preferred — beat-to-beat BP)
• Capnography (EtCO₂ — calibrate against PaCO₂; gradient usually 3–5 mmHg)
• Temperature probe
• Foley catheter (mandatory — osmotherapy causes diuresis)

• Invasive arterial line (radial artery) — essential for continuous MAP monitoring and ABG sampling
• ICP monitor if placed (see Part 6)
• Central venous access — for vasopressors and hypertonic saline >7.5%
• BIS/Processed EEG — depth of anaesthesia
• Neuromuscular monitoring (TOF) — especially to avoid coughing/bucking

7.4 Induction

• Pre-oxygenate thoroughly
• Avoid hypotension at induction — the commonest cause of secondary brain injury in the OR
• Attenuate laryngoscopy response — lignocaine IV, adequate depth before laryngoscopy
• Head-up 30° tilt maintained during induction if possible
• If RSI, use rocuronium + sugammadex available

7.5 Maintenance

7.6 Ventilation Strategy

"Hyperventilation should not be an automatic component of every neuroanesthetic. There should be an indication for its initiation. Hyperventilation has the potential to cause an adverse effect and should be withdrawn as the indication for it subsides." — Miller's Anesthesia, 10e (Chapter 53)

7.7 Fluid Management

"Although retrospective data analysis suggests that positive fluid balance is not associated with refractory intracranial hypertension, an association between hypervolemia and pulmonary edema was observed."

7.8 Blood Pressure Management

• Vasopressors of choice: Norepinephrine (noradrenaline) — maintains MAP without direct cerebral vasodilation
• Phenylephrine: Acceptable; may reflex bradycardia
• Avoid aggressive hypotension for haemostasis (permissive hypotension) — contraindicated in TBI
• If haemorrhage from fracture: maintain SBP ≥ 100–110 mmHg; avoid SBP < 90 mmHg absolutely

7.9 Positioning

• Head-up 30° — reduces ICP by facilitating venous drainage
• Avoid extreme neck rotation or flexion — obstructs jugular venous drainage → ↑ ICP
• Orthopaedic procedure (right leg): patient likely supine — generally compatible with head-up positioning
• Leg positioning: fracture table, skin traction, or standard table depending on fracture type

---

PART 8 — SPECIFIC ISSUE: FAT EMBOLISM SYNDROME (FES) — The Hidden Danger

"Intraoperative TEE has shown that most patients undergoing long-bone fracture manipulation experience microembolism of fat and marrow. After long-bone fractures, lung dysfunction occurs in almost all patients, ranging from minor laboratory abnormalities to fat embolism syndrome." — Miller's Anesthesia, 10e (Chapter 62)

Gurd's Criteria for FES Diagnosis

• Petechial rash (axillae, chest, conjunctivae — but only in 20–50% of cases)
• Respiratory insufficiency (PaO₂ < 60 mmHg on FiO₂ 0.4)
• Cerebral involvement (not attributable to other cause)

• Tachycardia > 110 bpm
• Pyrexia > 38.5°C
• Thrombocytopaenia
• High ESR
• Fat globules in urine/sputum
• Retinal changes (fat emboli in retinal vessels)
• Jaundice
• Renal changes

• CNS component of FES will be potentiated by pre-existing intracranial pathology
• Under GA, CNS changes will not be apparent — may manifest as failure to awaken post-surgery
• Any worsening of alveolar–arterial O₂ gradient + CNS deterioration → consider FES

• High FiO₂, high PEEP mechanical ventilation
• Supportive care
• Consider converting intramedullary nailing → external fixation to reduce embolic load
• For bilateral femur fractures: allow 1–2 days between successive nailing procedures

---

PART 9 — REGIONAL VERSUS GENERAL ANAESTHESIA DECISION

Box 62.8 & 62.9 — Miller's Comparison

• Allows continued neurological assessment (GCS monitoring maintained)
• Avoidance of airway instrumentation and pressure response
• Decreased blood loss
• Better postoperative mental status
• Lower incidence of DVT
• Improved postoperative analgesia

• Peripheral nerve function difficult to assess post-op
• Hemodynamic instability during placement → ↓ MAP → ↓ CPP (dangerous)
• Requirement for sedation (may cloud neurological assessment)
• May not be suitable if procedure prolonged
• Patient may not cooperate

• Speed of onset
• Duration — as long as needed
• Allows positive-pressure ventilation (ICP management)
• Multiple procedures possible

• Impairment of global neurologic examination (key concern)
• Requirement for airway instrumentation (pressor response risk)
• Haemodynamic management more complex

Recommendation for This Scenario

• Spinal / epidural (neuraxial) anaesthesia with judicious sedation (minimising doses) is possible — allows continued neurological monitoring
• Monitor carefully for sympatholysis-induced hypotension → have vasopressors ready

• General anaesthesia with TIVA (propofol + remifentanil) preferred
• Strict BP management with arterial line
• ICP monitor in situ if placed

---

PART 10 — INTRAOPERATIVE ICP RESCUE ALGORITHM

Box 53.4 — Methods for Rapid Reduction of ICP (After Checking Box 53.3)

1. First: Work through the Checklist (Box 53.3)
   • Jugular venous pressure — head rotation? Compression? Head-up?
   • Airway pressure — obstruction, bronchospasm, straining, pneumothorax, excessive PEEP?
   • PaCO₂ and PaO₂
   • Arterial pressure
   • Pain/arousal, seizures, fever?
   • Vasodilator drugs in use (N₂O, volatile agents, vasodilators)?
   • Unrecognised haematoma, expanding SDH, air + N₂O?
2. Rescue Measures (in escalating order):
   • Further reduce PaCO₂ to 23–25 mmHg (but not below!)
   • CSF drainage (EVD if in situ)
   • Diuresis (furosemide or mannitol)
   • CMR suppression: propofol bolus, barbiturates
   • MAP reduction (only if dysautoregulation confirmed)
   • Hyperosmolar therapy: mannitol 0.25–1 g/kg or hypertonic saline bolus
   • Surgical control (lobectomy / remove bone flap) — last resort

---

PART 11 — TREATMENT OF INTRACRANIAL HYPERTENSION — Stepwise Algorithm (Miller's Chapter 80)

---

PART 12 — OSMOTHERAPY SUMMARY

"HTS may provide superiority in the combined effect on intracranial pressure and CPP burden compared to mannitol in TBI, although a clear clinical outcome benefit has not been shown." NaCl > 7.5% causes endothelial damage — must be given via central vein only.

---

PART 13 — SPECIAL DRUG CONSIDERATIONS

---

PART 14 — EMERGENCE AND POST-OPERATIVE MANAGEMENT

Goals for Emergence

• Coughing, bucking, straining, Valsalva → acute ICP surge → herniation risk
• Extubate only when patient is fully awake and cooperative with intact airway reflexes
• OR: planned postoperative sedation and intubation in ICU if GCS declining or prolonged surgery

• Lignocaine 1 mg/kg IV 5 min before extubation
• Remifentanil infusion to extubation (titrated down slowly)
• Avoid sudden reversal of NMB (coughing risk)
• Dexmedetomidine infusion (0.4–0.7 mcg/kg/hr) — reduces coughing on emergence

Post-operative ICU/HDU Monitoring

• Hourly GCS assessment
• Continuous ICP monitoring (if monitor in situ)
• Maintain CPP 60–70 mmHg
• PaCO₂ 35–38 mmHg on ventilator
• Normothermia (antipyretics; cooling blanket)
• Normoglycaemia (BSL 6–10 mmol/L; avoid hypoglycaemia)
• DVT prophylaxis — mechanical (TED stockings, pneumatic compression) — chemical anticoagulation is contraindicated with SDH
• Strict intake/output with electrolytes monitoring (osmotherapy causes electrolyte shifts)
• Repeat CT head 24 hours post-op or any neurological deterioration

---

PART 15 — GLUCOSE AND TEMPERATURE MANAGEMENT

Glucose

Temperature

• Normothermia mandatory — fever ↑ CMR ~7% per °C → worsens ICP
• Induced hypothermia (32–34°C): NOT recommended as of current evidence
  • EUROTHERM trial: no outcome benefit
  • Multiple RCTs: negative
  • Current BTF: no established role for hypothermia in TBI management

---

PART 16 — ONE-PAGE SUMMARY TABLE FOR EXAM

---

REFERENCES (Miller's Anesthesia, 10e — Chapters Used)

• Chapter 53: Neuroanesthesia — ICP management, herniation, osmotherapy, PaCO₂, blood pressure, Box 53.1, 53.3, 53.4
• Chapter 53: ICP Monitoring for Non-Neurologic Surgery in the Brain-Injured Patient
• Chapter 43: Fluid Management — fluid choices in neurosurgery, HTS vs mannitol
• Chapter 62: Trauma Anaesthesia — fat embolism, long-bone fracture, GCS, RSI, regional vs general, Boxes 62.8, 62.9
• Chapter 80: Neurocritical Care — TBI treatment algorithm, CPP/ICP targets, sedation, stepwise ICP management

---

Bottom Line for the MD Anaesthesia Student: This patient is a neuroanesthetic high-wire act. Every drug choice, every ventilator adjustment, and every fluid bolus has a direct impact on ICP and CPP. The mantra is: "Protect the CPP, control the ICP, anticipate the secondary injury, and emerge smoothly." Never forget that the SDH with midline shift means the compensatory reserve is gone — there is no room for error.This comprehensive discussion is drawn entirely from Miller's Anesthesia, 10th Edition (Chapters 53, 43, 62, and 80). Here are the key take-home points structured for your MD exam:

---

Quick Recall Framework

The 3 Cardinal Questions Before This Anaesthetic

1. Is the ICP currently dangerous? (CT: midline shift = compensatory reserve depleted; GCS trend)
2. How much time since the SDH? (Delayed deterioration risk up to 4–4.5 days)
3. How long and demanding is the orthopaedic procedure? (Long surgery prone = higher ICP risk)

The Non-Negotiables

Scores to Know

• GCS (3–15): <8 = intubate; <15 + CT lesion = ICP monitor for surgery within 48h
• WFNS Scale (Grade 1–5): based on GCS + motor deficit
• Fisher/Modified Fisher Scale: CT grading of SAH blood (relevant if traumatic SAH component)
• ISS (Injury Severity Score): >15 = major trauma; FES more likely in high-ISS patients
• Gurd's Criteria and Schonfeld Score (≥5 points) for Fat Embolism Syndrome

The Unique FES Risk

---

Cadaveric Transplantation and Multiple Organ Procurement — Complete Anaesthetic Discussion

Miller's Anesthesia, 10th Edition

---

SECTION 1 — FRAMEWORK: TYPES OF CADAVERIC DONORS

1.1 Two Pathways to Cadaveric Donation

"Before the acceptance of brain death, all organs procured were from donors who suffered a cardiac demise (DCD, previously known as donation from a non-heart-beating donor). After the establishment of the Harvard criteria for brain death, DBD quickly became the principal source of organ donation." — Miller's Anesthesia, 10e (Chapter 57)

• In the USA (2021): DCD donors accounted for 30.2% of all deceased donors

---

SECTION 2 — BRAIN DEATH: DEFINITION, CRITERIA, DECLARATION

2.1 History and Legal Basis

• Harvard criteria (1968): First codification of brain death
• Brain death = Irreversible loss of ALL brain functions, including the brainstem
• Two functions that must be irreversibly lost:
  1. Capacity to breathe
  2. Capacity for consciousness

2.2 Prerequisites Before Brain Death Testing

1. Irreversible cause of neurological dysfunction must be established
2. Adequate systemic oxygenation and perfusion must be ensured
3. Confounders must be excluded and corrected:

2.3 Clinical Examination for Brain Death

2.4 Apnea Test

• Pre-oxygenate with 100% O₂ for 10 minutes
• Baseline ABG: PaCO₂ must be 35–45 mmHg (normocapnia)
• Disconnect from ventilator; deliver O₂ via tracheal catheter at 6 L/min
• Observe for respiratory movements for 8–10 minutes
• Repeat ABG at end: PaCO₂ must rise to ≥ 60 mmHg or ≥ 20 mmHg above baseline
• No respiratory effort = positive apnea test (supports brain death)

2.5 Ancillary / Confirmatory Tests

---

SECTION 3 — MAASTRICHT CLASSIFICATION OF DCD DONORS

Key point: Categories I and II = uncontrolled DCD (longer warm ischaemia time; higher risk). Categories III and IV = controlled DCD (most common in current practice).

DCD: Sequence After Life Support Withdrawal

1. Decision to withdraw life support made independently of transplant team
2. Comfort care medications (analgesia, anxiolytics) for patient
3. Trachea extubated; life support stopped
4. Death declared by physician not involved in transplantation
5. Duration between cardiac cessation and death declaration: 2–5 minutes (to confirm irreversibility)
6. Organ procurement begins immediately after declaration

University of Wisconsin (UW) DCD Prediction Score (Table 57.2)

---

SECTION 4 — PATHOPHYSIOLOGY OF BRAIN DEATH — TABLE 57.1

Miller's Table 57.1: Pathophysiologic Changes Associated with Brain Death

Two Phases of Cardiovascular Response to Brain Death

"Echocardiographic evidence of myocardial dysfunction is observed in 40% of brain-dead donors under consideration for heart donation."

---

SECTION 5 — ENDOCRINE DERANGEMENTS IN BRAIN DEATH

---

SECTION 6 — DONOR MANAGEMENT BEFORE PROCUREMENT

6.1 Haemodynamic Goals

"Adequate resuscitation, as evidenced by a MAP of 60–100 mmHg, may decrease cytokine levels and increase the number of organs available for transplantation."

6.2 Pulmonary Management (Lung Donor Protocol)

"Fluid restriction increases the number of lung grafts available for transplantation."

6.3 Hormonal Replacement Therapy (DBD Donors)

6.4 Electrolyte and Sodium Management

---

SECTION 7 — EXTENDED CRITERIA DONORS AND DONOR RISK INDICES

7.1 Standard Criteria Donor (SCD) vs Extended Criteria Donor (ECD)

"Donor risk is a relative term and should be best described as a continuum, not a dichotomy of SCD and ECD."

Box 57.1 — Kidney Donor Profile Index (KDPI) — 10 Variables

1. Age
2. Height
3. Weight
4. Ethnicity
5. History of hypertension
6. History of diabetes
7. Cause of death
8. Serum creatinine
9. Hepatitis C virus status
10. Donation after circulatory death (DCD)

KDPI scale: 1–100%. Higher KDPI = higher graft failure rate

Box 57.2 — Liver Donor Risk Index (DRI) — 8 Variables

1. Age (four categories: >40, >50, >60, >70 years)
2. Cause of death — CVA (lower risk) vs other
3. Race — African-American (higher risk) vs other
4. DCD — yes or no
5. Partial or split graft — yes or no
6. Height — increasing risk as height decreases below 170 cm
7. Regional or national share — yes or no
8. Cold ischaemia time

Clinical Implications of High-DRI/ECD Grafts for Anaesthesia

---

SECTION 8 — COLD ISCHAEMIA TIME: ORGAN-SPECIFIC LIMITS

"Cadaveric kidney transplantation is an urgent procedure since the ideal cold ischaemia goal for the kidney is under 24 hours."

Warm vs Cold Ischaemia

---

SECTION 9 — ANAESTHETIC MANAGEMENT OF THE CADAVERIC DONOR DURING PROCUREMENT SURGERY

9.1 Key Points (Chapter 57)

• Anaesthesia care required only for DBD donors (not DCD, except pre-mortem protocols)
• Majority of procurement occurs at community hospitals, not tertiary centres
• Surgical approach: midline laparotomy extended by sternotomy (wide exposure)
• Aortic cannula placed for cold preservation solution flush
• Ice applied to surgical field to protect organs

9.2 Order of Organ Removal (by ischaemic susceptibility)

9.3 Anaesthetic Drugs and Management

9.4 What Volatile Anaesthetics Offer in Procurement

"Volatile anaesthetics are commonly preferred since they may provide additional benefits that include ischaemic preconditioning and the reduction of ischaemia–reperfusion injury."

---

SECTION 10 — MELD SCORE (MODEL FOR END-STAGE LIVER DISEASE)

MELD Score Formula

"Many liver transplant allocation systems are based on the MELD score." — Miller's Key Points, Chapter 56

MELD-Na (Updated MELD)

• Incorporates hyponatraemia (a marker of portal hypertension severity)
• Higher MELD-Na → prioritised on transplant waiting list

---

SECTION 11 — KIDNEY TRANSPLANTATION: ANAESTHETIC MANAGEMENT

11.1 Preoperative Assessment

• ECG + history + physical for all candidates
• Active cardiac disease → cardiology review before transplant listing
• Asymptomatic high-risk candidates (diabetics, known CAD, poor functional capacity) → noninvasive CAD screening
• Asymptomatic known CAD: do NOT revascularise solely to reduce perioperative cardiac events
• Asymptomatic advanced triple-vessel CAD → may be excluded from transplant

"Many ESRD patients are deconditioned and unable to exercise. Scoring systems that use traditional CAD risk factors may underestimate the risk of occult CAD in ESRD patients."

11.2 Urgency

• Cadaveric kidney transplant is an URGENT procedure — cold ischaemia goal < 24 hours
• Living donor transplant = scheduled elective surgery

11.3 Intraoperative Goals

11.4 Delayed Graft Function (DGF)

• Defined as: need for dialysis within first week post-transplant
• Higher incidence with: DCD grafts, ECD kidneys, prolonged cold ischaemia, large-dose HES in donor
• Large doses of starch-based colloids in donors → associated with DGF

---

SECTION 12 — LIVER TRANSPLANTATION: ANAESTHETIC MANAGEMENT

12.1 Three Surgical Stages — The Anaesthetist's Framework

12.2 Post-Reperfusion Syndrome (PRS)

• Definition: ≥ 30% decrease in MAP from baseline, persisting for at least 1 minute, within the first 5 minutes after reperfusion
• Mechanism: Efflux of cold, hyperkalaemic, acidic preservation solution from graft into systemic circulation
• Complications: Hypotension, bradycardia, asystole, hyperkalemia, arrhythmias
• Prevention/Treatment: Calcium chloride before reperfusion; bicarbonate; insulin/glucose for K⁺; vasopressors; reperfusion slowly

12.3 Rapid Sequence Induction (RSI) — Mandatory

• All LT patients are at elevated aspiration risk:
  • Delayed gastric emptying (ESLD)
  • Ascites
  • Preoperative oral immunosuppressants/antibiotics
• RSI is standard induction technique for all liver transplants

12.4 Vascular Access for Liver Transplant

"A rapid infusion system capable of high transfusion flow rates (approximately 500 mL/min) connected to a large-bore central venous catheter is standard."

12.5 Electrolyte Monitoring During Liver Transplant

12.6 Coagulation Management in Liver Transplant

"Administration of blood products and/or factor concentrates during liver transplantation should be reserved only for clinically significant bleeding; prophylactic administration is not recommended."

12.7 Post-Liver Transplant Survival Data

---

SECTION 13 — ACUTE LIVER FAILURE (ALF): SPECIAL CONSIDERATIONS

Definition

• Encephalopathy + coagulopathy (INR ≥ 1.5) in a patient without prior liver disease with illness < 26 weeks duration

Incidence

• ~1 case per million per year; ~2000–3000 cases/year in the USA

Prognosis by Aetiology

ALF Anaesthetic Management Points

• Cerebral oedema with intracranial hypertension is the most lethal complication
• Head-up 30°, neutral neck position to reduce ICP
• Intubation + controlled ventilation for GCS decline or encephalopathy
• Mannitol for osmotic diuresis (limited utility in renal compromise)
• Plasma exchange / MARS (molecular adsorbent recirculating system) as bridge to transplant
• Overall survival ALF: now >70% with modern care and transplantation

---

SECTION 14 — HEART TRANSPLANTATION

14.1 Indications (Paediatric — Chapter 73)

14.2 Pulmonary Vascular Resistance (PVR) Thresholds

"Most adult transplant programs will not offer heart transplant therapy to patients with PVR over 6 Wood units/m²."

14.3 Anaesthetic Management Principles for Heart Transplant

• Careful titration of anaesthetic agents with minimal myocardial depressant characteristics
• Avoid excessive opioids — can cause cardiovascular deterioration by reducing endogenous catecholamines
• Airway and ventilation management critical in presence of elevated PVR
• For Trendelenburg position for central line: may not be tolerated by decompensated patients — use level table + ultrasound

---

SECTION 15 — LUNG DONOR CONSIDERATIONS (DCD vs DBD)

---

SECTION 16 — PANCREAS TRANSPLANTATION

Types

• SPK: Simultaneous Pancreas-Kidney transplant (most common — diabetic nephropathy)
• PAK: Pancreas after Kidney
• PTA: Pancreas Transplant Alone (brittle diabetes)

Preoperative Evaluation (Chapter 56)

• Indication: definitive treatment for diabetes mellitus (including combined kidney transplantation in diabetic patients with renal failure)
• High cardiovascular risk in diabetics — same KDIGO cardiac evaluation principles apply
• Silent ischaemia more common in diabetics with ESRD

Anaesthetic Management Key Point

• Close monitoring of blood glucose levels — perioperative requirement specific to pancreas transplant
• Risk of hyperglycaemia (donor-related), then hypoglycaemia after reperfusion of functioning graft

---

SECTION 17 — SUMMARY: ORGAN ALLOCATION SCORES AND INDICES

---

SECTION 18 — ONE-PAGE EXAM SUMMARY TABLE

---

REFERENCES — Miller's Anesthesia, 10e Chapters Used

• Chapter 57: Organ Donation and Procurement — Table 57.1, Table 57.2, Box 57.1, Box 57.2; brain death; DCD; Maastricht classification; UW score; donor management
• Chapter 56: Anaesthesia for Abdominal Organ Transplantation — MELD, kidney, liver, pancreas, intestinal transplantation; KDIGO guidelines; three phases of LT
• Chapter 73: Paediatric Cardiac Anaesthesia — Heart transplantation PVR thresholds
• Chapter 80: Neurocritical Care — Brain death declaration criteria and ethics

---

Examiner's Perspective: The highest-yield areas for MD anaesthesia exams in this topic are: (1) Table 57.1 incidence figures for brain death pathophysiology, (2) Maastricht classification and UW Score, (3) MELD score and its surgical risk implications, (4) three phases of liver transplantation and post-reperfusion syndrome, (5) organ-specific cold ischaemia times, and (6) procurement anaesthesia — neuromuscular blockers for spinal reflexes, isoproterenol for bradycardia, and the role of volatile anaesthetics.This is a complete, exam-ready discussion drawn entirely from Miller's Anesthesia, 10th Edition (Chapters 56, 57, 73, 80). Here's your quick orientation to the structure:

---

How to Use This for Exam Preparation

1. Brain Death — Harvard criteria (1968), prerequisites, clinical exam, apnea test (PaCO₂ must rise to ≥60 mmHg), ancillary tests, and the critical distinction between DBD and DCD
2. Maastricht Classification (I–IV) + UW DCD Score (8–24) — These scores define the DCD donor pool and predict organ usability; Maastricht III & IV = controlled DCD (most used)
3. Pathophysiology of Brain Death (Table 57.1) — The incidence figures are high-yield: hypertension AND hypotension both at 80–90%, DI at 45–90%, DIC at 30–55%. The two-phase cardiovascular response (catecholamine storm → vasoplegia) drives all donor management decisions
4. MELD Score — The cornerstone of liver allocation and a direct predictor of surgical complexity; MELD >35 = high-risk anaesthesia territory with mandatory massive transfusion preparedness
5. Procurement Anaesthesia — Only for DBD; organs removed heart-first, kidneys-last; atropine DOES NOT WORK for bradycardia (use isoproterenol); neuromuscular blockers for spinal reflexes; volatile agents preferred (ischaemic preconditioning benefit); heparin before cross-clamping

Miller's Anesthesia, 10th Edition — Complete Discussion

---

UNPACKING THE CLINICAL SCENARIO

• Mechanism: Road Traffic Accident (RTA) → polytrauma, full stomach assumed, possible cervical spine injury
• Intracranial injuries: Subdural Haematoma (SDH) + Subarachnoid Haemorrhage (SAH) — traumatic
• Neurological status: GCS E4V3M6 = Total 13
• Planned surgery: Decompressive craniotomy (evacuation of SDH + decompression)

---

PART 1 — SCORING SYSTEMS AND CLASSIFICATIONS

1.1 Glasgow Coma Scale — Detailed Breakdown

• V3 (inappropriate words) — confused, not oriented
• Being rushed for decompressive craniotomy → rapid neurological deterioration expected
• Any GCS decline below 9 while in your care → intubation is mandatory without further delay
• "Patients can talk and deteriorate, or talk and die" after TBI with LOC — Miller's explicit warning

"Patients with good scores can talk and deteriorate or talk and die after a TBI associated with loss of consciousness. Delayed deterioration has been observed as much as 4 days after the initial injury." — Miller's Anesthesia, 10e (Chapter 53)

1.2 World Federation of Neurological Surgeons (WFNS) Scale

Higher WFNS grade = worse clinical outcome

1.3 Hunt–Hess Classification (SAH — Table 53.3, Miller's)

"Serious systemic disease such as hypertension, diabetes, severe arteriosclerosis results in placement of the patient in the next less-favourable category." — Miller's footnote to table

1.4 Fisher / Modified Fisher Scale — CT Classification of SAH

"The highest incidence of vasospasm is observed in patients with modified Fisher grade 4."

1.5 Traumatic SAH Epidemiology

"Traumatic SAH (tSAH) occurs in up to 60% of admissions for TBI and influences outcome. Approximately 20% of patients with tSAH may also develop vasospasm, which causes secondary ischaemic insult." — Miller's Anesthesia, 10e (Chapter 80)

1.6 TBI Severity Classification

"Severe TBI is classified as GCS ≤ 8 at admission and carries significant mortality. Patients with severe TBI have mortality three times that of patients with other types of traumatic injury."

---

PART 2 — PATHOPHYSIOLOGY: PRIMARY AND SECONDARY BRAIN INJURY

2.1 Primary Injury

• Direct mechanical injury at time of impact: axonal shearing, cortical laceration, haematoma
• Cannot be influenced by therapy — prevention (helmets, airbags) is the only protection

2.2 Secondary Brain Injury — What the Anaesthetist Targets

"A single episode of hypoxaemia (PaO₂ < 60 mmHg) occurring in a patient with severe TBI can double the incidence of mortality."

"A single episode of hypotension (SBP < 90 mmHg) is associated with an increase in morbidity and doubled mortality after severe TBI."

2.3 CBF Pattern After TBI

---

PART 3 — PREOPERATIVE ASSESSMENT AND PREPARATION

3.1 Immediate Assessment — ABCDE + Neurological Exam

3.2 Pupil Assessment — Herniation Warning Signs

3.3 Cushing's Triad — Impending Brainstem Herniation

3.4 Preoperative Investigations

3.5 SAH-Associated Cardiac Changes — Critical for Anaesthetist

"Troponin elevation occurs commonly, though typically reaching levels less than the diagnostic threshold for myocardial infarction. Peak troponin levels correlate with the severity of both neurologic injury and echocardiographic dysfunction."

"An increased QTc interval (> 550 msec) occurs frequently after SAH and has been associated with an increased incidence of malignant ventricular rhythms including torsades de pointes."

• Subendocardial ischaemia → biventricular failure
• Even in young, previously healthy patients
• β-adrenergic blockade may be protective

---

PART 4 — AIRWAY MANAGEMENT

4.1 Challenges Specific to This Patient (Box listing — Miller's Chapter 53)

4.2 Technique: Modified RSI with In-Line Stabilisation

• Rapid Sequence Induction (RSI) — standard approach for all trauma patients with full stomach + TBI
• In-line axial stabilisation (not traction) — limits atlanto-occipital extension
• Back half of cervical collar may be left in place — acts as strut, limits extension
• Cricoid pressure applied

"Although in-line stabilisation properly performed makes laryngoscopy more difficult, it serves to decrease the amount of atlanto-occipital extension necessary to achieve visualisation of the glottis."

"In a resuscitation situation, before initiating a hypnotic-relaxant sequence, confirm the availability of cricothyrotomy equipment."

4.3 RSI Drug Choices for This Patient

"The necessity to use succinylcholine in these circumstances has diminished with the availability of both rocuronium and the reversal agent sugammadex." — Miller's

"As is the case in many other situations, the laryngeal mask may be a very useful device for temporising in the face of a failed intubation and may also provide access for intubation as an alternative to cricothyrotomy."

4.4 Cervical Spine Management

• Modern multislice CT alone is sufficient to rule out unstable bony cervical spine injuries
• MRI may identify ligamentous injury CT misses — but in emergency, clinical urgency prevails
• Cricothyrotomy/tracheostomy rate at major trauma centre (Cowley Shock Trauma Centre): 0.3%
• Video laryngoscope reduces need for head extension — preferred in RTA patients

---

PART 5 — INTRAOPERATIVE MONITORING

"The anesthesiologist should appreciate that the priority is to open the cranium as rapidly as possible. After achieving IV access, the risks and benefits of delaying craniotomy for line placement should be considered carefully. An arterial line, often placed after induction in urgent situations, is appropriate for essentially all acute trauma craniotomies."

"Sudden hypotension after dural opening with high ICP can occur as brainstem compression is relieved. Appropriate intravascular volume resuscitation should mitigate this occurrence."

---

PART 6 — HAEMODYNAMIC TARGETS AND BLOOD PRESSURE MANAGEMENT

6.1 Non-Negotiable Targets

6.2 SAH-Specific Blood Pressure

"Absolute avoidance of acute hypertension with its attendant risk of rebleeding." "Maintenance of a high-normal MAP to prevent critical reduction of CBF in recently insulted and now marginally perfused areas of brain."

• Target MAP high-normal
• Hypotension is the enemy (vasoconstriction from tSAH may already compromise CBF)
• Pressor augmentation target: increase MAP by 20–30 mmHg above baseline SBP

6.3 Three BP Management Concepts (Miller's Chapter 53)

---

PART 7 — ANAESTHETIC TECHNIQUE FOR DECOMPRESSIVE CRANIOTOMY

7.1 Drug Selection Principles

"Craniotomies are most commonly performed for the evacuation of subdural, epidural, or intracerebral haematomas. In general, anaesthetics that are known to be cerebral vasoconstrictors are preferable to those that have the potential to dilate the cerebral circulation."

"When the ICP is out of control (or unknown), or the surgical field is tight, omitting the inhaled anaesthetics in favour of intravenous agents is appropriate."

"For patients who are likely to remain intubated post-operatively, an anaesthetic based primarily on a narcotic, such as fentanyl, and a muscle relaxant usually serves well."

7.2 Recommended Anaesthetic Plan

• Pre-oxygenation × 5 min
• Fentanyl 2 mcg/kg + Lignocaine 1.5 mg/kg IV (3 min before)
• Propofol 1.5–2 mg/kg (titrated, watch BP) + Rocuronium 1.2 mg/kg
• Cricoid pressure + in-line stabilisation
• Video laryngoscope preferred

• TIVA preferred: Propofol infusion (4–8 mg/kg/hr) + Remifentanil infusion (0.05–0.2 mcg/kg/min)
• Alternative: Sevoflurane < 1 MAC + Fentanyl infusion (NO N₂O)
• BIS-guided depth (target BIS 40–60)
• Rocuronium infusion or repeat bolus (TOF-guided)

---

PART 8 — VENTILATION STRATEGY

"Hyperventilation to PaCO₂ of 25 mm Hg, long a mainstay of managing TBI, is no longer recommended as prophylactic treatment. A range of PaCO₂ between 30 and 35 mmHg should be induced only for episodes of increased ICP that cannot be controlled with other means."

---

PART 9 — ICP MANAGEMENT (INTRAOPERATIVE)

Box 53.3 — "Tight Brain" Checklist (Applied Intraoperatively)

• Jugular venous pressure — head rotation? Extreme neck flexion? Head-up position maintained?
• Airway pressure — obstruction, bronchospasm, coughing/straining, pneumothorax, excessive PEEP?
• PaCO₂ and PaO₂ — normalised?
• Arterial pressure — MAP adequate?

• Pain/arousal adequate?
• Seizures occurring?
• Febrile?

• N₂O? Volatile agents at high concentration? Nitroprusside? Calcium channel blockers?

• Expanding SDH? Intracerebral haematoma? Air ± N₂O?

Box 53.4 — Rapid ICP Reduction Measures (Escalating Order)

1. Further reduce PaCO₂ to 23–25 mmHg (not below)
2. CSF drainage — EVD open if in situ
3. Diuresis — furosemide
4. CMR suppression — propofol bolus, barbiturate
5. MAP reduction (only if dysautoregulation proven)
6. Hyperosmolar therapy:
   • Mannitol 0.25–1 g/kg IV over 10–15 min
   • HTS bolus (3%, 7.5%, or 23.4% via central line)
7. Surgical control — remove bone flap (the procedure itself is the ultimate ICP rescue)

Brain Relaxation for Decompressive Craniotomy

"Surgeons who believe in CBF-enhancing effect of mannitol may request a second 1 g/kg approximately 15 minutes before anticipated temporary occlusion."

---

PART 10 — OSMOTHERAPY: MANNITOL vs HYPERTONIC SALINE

"Mannitol should be administered by infusion (e.g., over 10–15 minutes). Sudden exposure to extreme hyperosmolarity can have a vasodilatory effect, causing brain engorgement and increased ICP."

---

PART 11 — FLUID MANAGEMENT

Haemoglobin and TBI

"A haemoglobin lower than 7 g/dL results in impaired brain function and a haemoglobin lower than 10 g/dL may be detrimental to recovery from TBI."

---

PART 12 — TRAUMATIC SAH-SPECIFIC CONSIDERATIONS

Vasospasm After Traumatic SAH

• Incidence: ~20% of tSAH patients develop vasospasm
• Timing: peaks 4–14 days after SAH
• Risk higher with: large blood clot (Fisher 3–4), IVH, thick SAH
• Monitoring: TCD (transcranial Doppler), CT perfusion, cerebral angiography, cEEG (in high-grade patients)

Treatment of Vasospasm / DCI

SIADH vs Cerebral Salt Wasting (CSW) After SAH

"Fluid restriction and further volume contraction may be especially deleterious in the post-SAH patient and should be avoided."

---

PART 13 — DECOMPRESSIVE CRANIOTOMY — SURGICAL AND ANAESTHETIC SPECIFICS

Indications for Decompressive Craniectomy

"Decompressive craniectomy is indicated for selected anatomic patterns of TBI, such as when CPP cannot be maintained despite the vigorous application of the previously described therapies, including barbiturate coma."

Miller's Warning on Decompressive Craniectomy

"Decompressive craniectomy has been a strategy to lower ICP, but unfortunately this intervention increases the number of patients surviving in a vegetative state or with severe brain damage."

"The updated recommendations of the Brain Trauma Foundation (BTF) now suggest decompressive craniectomy only in patients with late refractory increased ICP, but not in patients with early refractory increased ICP."

Haemodynamic Events at Dural Opening

---

PART 14 — BLOOD PRESSURE MANAGEMENT IN COMBINED SDH + TRAUMATIC SAH

"For patients proceeding to surgery, hypotension should be avoided and CPP should usually be maintained intraoperatively at values near the waking normal range."

• Norepinephrine — preferred; maintains MAP without direct cerebral vasodilation
• Phenylephrine — pure α₁-agonist; acceptable; may cause reflex bradycardia
• Dopamine — second-line; may cause arrhythmias, especially with SAH-related cardiac changes
• Phenylephrine and dopamine — most commonly used pressors in SAH per Miller's

---

PART 15 — EMERGENCE AND POSTOPERATIVE PLAN

Extubation Decision

"For patients who are likely to remain intubated post-operatively, an anaesthetic based primarily on a narcotic (fentanyl) and a muscle relaxant usually serves well."

Smooth Emergence (If Extubating)

• Lignocaine 1 mg/kg IV 5 min before extubation
• Remifentanil titration to extubation
• Dexmedetomidine 0.4–0.7 mcg/kg/hr — reduces coughing
• Extubate only when fully awake and cooperative
• Avoid Valsalva, bucking, sudden hypertension

ICU Post-op Management

---

PART 16 — IMPORTANT SUMMARY: "MUST KNOWS" FOR MD EXAM

Critical Numbers at a Glance

---

REFERENCES — Miller's Anesthesia, 10e

• Chapter 53: Neuroanesthesia — ICP control, SAH anaesthetic technique, Hunt-Hess, WFNS, Fisher scales, airway challenges in TBI, osmotherapy, brain protection, Boxes 53.1/53.3/53.4, Tables 53.1/53.3
• Chapter 62: Trauma Anaesthesia — Decompressive craniectomy indication, TBI management algorithm, RSI, cervical spine, haemoglobin targets, ARDS + TBI double-hit
• Chapter 80: Neurocritical Care — Traumatic SAH incidence/vasospasm, TBI pathophysiology/treatment, CPP/ICP stepwise algorithm, CSWS vs SIADH, Box 80.3, Tables 80.3/80.4/80.8/80.9

---

One-Line Clinical Rule for this Patient: GCS 13 with SDH + tSAH going for decompressive craniotomy = treat as deteriorating severe TBI; RSI with rocuronium; TIVA propofol; NO N₂O; NO hypotension; NO steroids; NO albumin; normocapnia unless herniating; mannitol before dural opening; plan for ICU intubated post-op; start nimodipine for 21 days.Your credits are exhausted. Your daily credits reset tomorrow, or you can purchase a top-up for more.