Upper Extremity Regional Blocks: Comprehensive Q&A

PART I — BRACHIAL PLEXUS ANATOMY

PART II — INTERSCALENE BLOCK

• Absolute: Bilateral interscalene blocks (bilateral phrenic palsy → apnea); contralateral phrenic nerve palsy; severe pulmonary disease (e.g., moderate-to-severe COPD) — hemidiaphragmatic paresis can cause dyspnea, hypercapnia, and hypoxemia; local anesthetic allergy; local infection; patient refusal
• Relative: Contralateral vocal cord paralysis (recurrent laryngeal nerve block → respiratory distress); coagulopathy; obesity (worsens diaphragmatic impact)

1. Reduce volume to ≤5–10 mL (US-guided)
2. Anterior suprascapular nerve block — targets the suprascapular nerve at the omohyoid for shoulder analgesia without significant phrenic involvement
3. Superior trunk block — selective deposition at the superior trunk distal to phrenic nerve origin
4. Low interscalene block (just above clavicle, below C6)

PART III — SUPRACLAVICULAR BLOCK

PART IV — INFRACLAVICULAR BLOCK

• Complete brachial plexus anesthesia
• Stable catheter location — the infraclavicular region is the optimal approach for continuous peripheral nerve catheters
• No arm manipulation required
• Low phrenic nerve risk (below the level of phrenic nerve origin)
• The cords are at predictable positions relative to the axillary artery

• Deep block — beneath pectoralis major and minor; steep needle angles reduce tip visibility
• Slower onset than axillary block
• Requires either probe manipulation or steep needle angulation

• Lateral cord → 10 o'clock (lateral/superior to artery)
• Posterior cord → 6 o'clock (directly posterior)
• Medial cord → 4 o'clock (medial/inferior)

• Reduction in axillary artery diameter during injection
• "U-shaped" LA distribution underneath the artery
• Separation of cords from the axillary artery
• "White wall" appearance to the artery (free walls)
• Dark layer underneath the artery on long-axis view

PART V — AXILLARY BLOCK

• Safest brachial plexus approach — superficial, compressible, no phrenic nerve risk, no pneumothorax
• Suitable for anticoagulated patients
• No risk of spinal/epidural injection

• Musculocutaneous nerve has already left the axillary sheath proximal to the axilla → must be blocked separately
• Intercostobrachial nerve (T2 — medial upper arm) must be blocked separately for tourniquet tolerance
• Requires arm abduction to 70–90° with elbow flexion — not possible in severe trauma or frozen shoulder
• Fascial septa within the axillary sheath create separate compartments → single injection is unreliable → multi-injection technique required
• Low catheter success rate vs. infraclavicular

• Median nerve — anterior/superior (12 o'clock)
• Ulnar nerve — posterior-inferior and medial
• Radial nerve — posterior-inferior and lateral
• Musculocutaneous nerve — within or adjacent to the coracobrachialis muscle lateral to the bundle. Characteristic shape: round when adjacent to artery → flat inside coracobrachialis → triangular on exit. Must be identified and injected separately.

• Above artery → Median (wrist/finger flexion, pronation) and musculocutaneous (elbow flexion)
• Below artery → Ulnar (ring/little finger flexion, ulnar wrist deviation) and radial (wrist/finger extension)

PART VI — ELBOW BLOCK

1. Intraneural injection — fascicles may be directly entered in the confined space
2. Elevated tunnel pressure — local anesthetic volume cannot decompress
3. Post-block ulnar neuropathy (weakness, clawing, sensory loss in little/ring finger)

PART VII — WRIST BLOCK

• Insert needle just radial to the PL tendon at the proximal wrist crease
• Depth ~3–5 mm
• Inject 3–5 mL after negative aspiration
• Avoid epinephrine (end-artery territory of digital vessels)

• Insert needle just medial to the pulsating ulnar artery, lateral to FCU
• Inject 3–5 mL after careful aspiration (ulnar artery is immediately adjacent)
• US Doppler is valuable to avoid arterial puncture

• 3–5 mL deposited subcutaneously in a band across the dorsal wrist from the radial artery to the dorsum
• At the level of the radial styloid

PART VIII — FOREARM BLOCKS

1. Supplement an incomplete brachial plexus block — targeted rescue of missed segments
2. Selective anesthesia for limited-field procedures (single digit)
3. Avoid proximal block complications — no phrenic nerve palsy, pneumothorax, or Horner syndrome
4. Safest ulnar nerve approach — midforearm avoids cubital tunnel pressure injury risk
5. Technically easy with US — all nerves are superficial (<2 cm)
6. Smaller LA volumes — lower LAST risk

• OOP: Needle perpendicular at 45–60°; center nerve on screen
• IP (medial-to-lateral) at elbow: Allows tracking to avoid brachial artery

• "Hockey stick" small-footprint linear probe preferred at the distal forearm
• Inject at the most proximal point where the nerve is still clearly separate from the ulnar artery
• IP technique with needle aligned to the probe, approaching laterally
• Volume: 5 mL; circumferential spread; avoid arterial puncture

• US: flat hypoechoic nerve within the coracobrachialis muscle; inject 5 mL directly within the muscle belly

• Subcutaneous injection of 5–10 mL in the lateral bicipital groove anesthetizes the nerve between biceps and brachialis

PART IX — LOCAL ANESTHETIC SELECTION AND DOSING

PART X — TOXICITY AND SAFETY

1. Stop injection immediately
2. Airway — 100% O₂, intubation if needed (hypoxia/acidosis worsen toxicity)
3. Benzodiazepines for seizure suppression
4. Lipid emulsion rescue (Intralipid 20%): Bolus 1.5 mL/kg IV → infusion 0.25 mL/kg/min; repeat bolus 1–2× if no improvement
5. ACLS for cardiac arrest; avoid vasopressin, calcium channel blockers, beta-blockers
6. Prolonged CPR may be required

PART XI — ULTRASOUND PRINCIPLES

1. Nerve appearance: In short axis — honeycomb pattern (hypoechoic fascicles in hyperechoic epineurium). In long axis — parallel hyperechoic lines.
2. Frequency: 10–15 MHz for superficial nerves (axillary, forearm, wrist); lower for deep blocks (infraclavicular in obese).
3. In-plane (IP): Full needle visibility — preferred for deep or high-risk blocks.
4. Out-of-plane (OOP): Only needle cross-section visible — acceptable for superficial blocks.
5. Color Doppler: Identify adjacent vessels before needle advancement.
6. D5W hydrodissection: Identifies perineural space without interfering with NS response.
7. Intraneural injection sign: Nerve cross-sectional area increases during injection → stop immediately.

PART XII — ADVANCED TOPICS

1. Superior trunk block — LA deposited at superior trunk distal to C5's phrenic contribution; provides shoulder analgesia via suprascapular and axillary nerves
2. Anterior suprascapular nerve block — at the omohyoid; blocks ~70% of shoulder joint afferents
3. Low-volume ISB (≤5 mL) — reduces but does not eliminate phrenic block
4. Combined suprascapular + axillary nerve block — covers shoulder without phrenic nerve

• Anterior approach: Deep to omohyoid in posterior triangle; 5–10 mL
• Posterior approach: In supraspinous fossa; patient sitting/lateral; 5–10 mL

MASTER SUMMARY TABLE

Anaesthetic Management of the Diabetic Patient

Comprehensive Q&A from Miller's Anesthesia 10e & Barash Clinical Anesthesia 9e

SECTION A — FOUNDATIONS: DIABETES AND ANAESTHESIA

• Macrovascular: Coronary artery disease, hypertension, cerebrovascular disease, peripheral vascular disease
• Microvascular: Retinopathy, nephropathy, neuropathy (peripheral and autonomic)
• Other: Stiff joint syndrome, gastroparesis, increased infection risk, poor wound healing

1. Type 1 diabetes — Immune-mediated β-cell destruction; absolute insulin deficiency
2. Type 2 diabetes — Progressive insulin resistance with variable secretory defect; accounts for the great majority of diabetics
3. Secondary diabetes — Due to glucocorticoids, HIV medications, post-transplant immunosuppressants, chronic pancreatitis/pancreatectomy, or monogenic syndromes (maturity-onset diabetes of the young — MODY)
4. Gestational diabetes (GDM) — Diagnosed during second or third trimester in a previously non-diabetic patient; highly relevant for the LSCS scenario

• Diabetics (especially insulin-requiring) are categorised as "elevated risk" for perioperative cardiac events under the 2014 ACC/AHA Guidelines — Barash p. 4046

• Target HbA1c for Type 1 DM: <8% (ADA) — delay elective surgery if above
• Target HbA1c for Type 2 DM: <7% (ADA) — delay elective surgery if above
• If HbA1c is above target range, elective surgery should be postponed for optimisation — Barash p. 4062

• Predominantly Type 1 DM (also SGLT-2 inhibitor-associated euglycaemic DKA in Type 2)
• Blood glucose: 250–400 mg/dL (moderate elevation)
• Ketonemia: elevated β-hydroxybutyrate, acetoacetate, acetone
• Metabolic acidosis with increased anion gap
• Volume deficit: approximately 2–4 L
• pH: <7.3 (usually); HCO₃: <18 mEq/L

• Predominantly Type 2 DM, older patients
• Blood glucose: 600–1000 mg/dL (markedly elevated)
• No ketosis (sufficient residual insulin to prevent lipolysis)
• No significant acidosis
• Volume deficit: 6–10 L (much greater than DKA)
• Osmolality: markedly elevated
• Mortality: 10–20% (Barash) vs. DKA mortality ~1–5% (Miller gives DKA mortality 5%, HHS mortality 10–20%)
• Coma, seizures, intravascular thrombosis due to hyperviscosity

• SGLT-2 inhibitors must be discontinued 3–4 days before surgical procedures to prevent ketoacidosis
• These patients may have DKA with a blood glucose that appears deceptively normal — check ketones

SECTION B — SCENARIO 1: 40-YEAR-OLD DIABETIC FOR SHOULDER SURGERY UNDER GENERAL ANAESTHESIA

1. History

• Type of diabetes (Type 1 vs Type 2) and duration
• Current diabetes medications: Insulin regimen (type, dose, timing), OHAs (particularly metformin and SGLT-2 inhibitors)
• Glycaemic control history: Frequency and severity of hypoglycaemic episodes; level at which symptoms occur; hypoglycaemic unawareness?
• HbA1c: Most recent value and trend
• Insulin pump users: Pump type, basal rate, insulin-to-carbohydrate ratio, correction factor, glucose targets

2. Systemic Review for Diabetic Complications

• History of CAD, MI, angina, heart failure, hypertension
• ECG: silent ischemia (common due to autonomic neuropathy — diabetics may have no symptoms)
• Echocardiogram if symptomatic or abnormal ECG

• Orthostatic hypotension, resting tachycardia, exercise intolerance
• Gastroparesis — nausea, vomiting, early satiety, bloating → aspiration risk even after adequate fasting
• Decreased hypoxia-induced ventilatory drive
• Baroreceptor insensitivity → haemodynamic lability during anaesthesia

• Pre-existing neurological deficits — must be documented before any regional technique or positioning
• Vascular disease → increased susceptibility to positioning injuries

• Creatinine, eGFR, urine albumin/creatinine ratio — diabetic nephropathy → contrast precautions, drug dose adjustments
• Microalbuminuria rises logarithmically at HbA1c >8% — Miller p. 4587

• Stiff joint syndrome — glycosylation of proteins + abnormal collagen cross-linking → reduced mobility of temporomandibular joint, atlanto-occipital joint, and cervical spine → difficult intubation
• Particularly in longstanding Type 1 DM; incidence of difficult intubation 20–30% in some series (Barash)
• "Prayer sign": Inability to completely oppose palmar surfaces of interphalangeal joints — traditionally associated with stiff joint syndrome and difficult laryngoscopy. Miller (p. 4591) notes this has been refuted as a predictor of difficult laryngoscopy but Barash (p. 2841) states it may predict difficult laryngoscopy in up to 40% of juvenile DM patients presenting for renal transplantation
• Thorough airway exam mandatory before induction for all diabetic patients

3. Preoperative Laboratory Investigations

• Blood glucose (on arrival and 1-hourly if delayed)
• HbA1c (target: Type 1 <8%, Type 2 <7%)
• Serum electrolytes (K⁺ critical — OHAs and DKA affect potassium)
• Creatinine and eGFR
• ECG (12-lead — screen for silent ischaemia)
• Urinalysis/urine dipstick — ketonuria, proteinuria
• Fasting lipid profile if not recent (for cardiovascular risk)

Oral Hypoglycaemic Agents

Insulin Regimens on Day of Surgery

• Never withhold ALL insulin → risk of DKA
• Evening before surgery: Continue usual dose of short-acting insulin with the evening meal; reduce intermediate/long-acting by 20%
• Morning of surgery: Omit morning short-acting insulin; reduce intermediate-acting by 50% or long-acting by 20% (give only if fasting glucose >120 mg/dL — Barash p. 2850)
• Maintain a 5% dextrose infusion at 75–125 mL/hour to prevent hypoglycaemia while fasting

• Hold oral agents; manage with insulin infusion or basal long-acting insulin + regular insulin sliding scale (RISS)
• A RISS as the sole method of control is discouraged (Barash p. 2990) — risk of wide glucose fluctuations

• Continue pump intraoperatively with basal rate reduced by 20–25%
• Check blood glucose every hour if pump is continued during surgery — Barash p. 2850

1. Schedule as the first case of the day — to minimise fasting duration (Barash p. 4080)
2. Patient arrives in early morning — blood glucose checked on arrival and every hour if the case is delayed
3. If hypoglycaemia develops during waiting: Give glucose tablet or clear juice (oral) if no IV; IV glucose-containing fluid if IV is in place
4. Coordinate preoperative optimisation with the patient's endocrinologist 1–2 weeks before elective surgery (Barash p. 4060)
5. Type 1 diabetics should be first case to minimise the risk of DKA from prolonged fasting

A. Airway Management

• Thorough airway evaluation for stiff joint syndrome — reduced TM joint and atlanto-occipital mobility
• Use the prayer sign as part of the preoperative airway assessment
• Prepare for potential difficult intubation: Have fibreoptic equipment, video laryngoscope, and airway trolley available
• Patients with acromegaly (associated with DM) have 20–30% incidence of difficult intubation

B. Aspiration Risk

• Gastroparesis from autonomic neuropathy → delayed gastric emptying → residual gastric contents even after adequate fasting
• Increase index of suspicion; consider RSI (rapid sequence induction) if gastroparesis is confirmed
• GLP-1 receptor agonists further delay gastric emptying — particularly risky if recently started
• Consider premedication with metoclopramide, H₂-blocker or PPI, and sodium citrate

C. Positioning: Beach Chair or Lateral Decubitus

• Shoulder surgery is most commonly performed in the beach chair position (sitting/semi-recumbent)
• Haemodynamic implications for the diabetic:
  • Autonomic neuropathy → orthostatic hypotension — diabetics are at heightened risk of severe hypotension in the upright position, which may worsen silent cardiac ischaemia
  • Cerebral hypoperfusion — cerebral perfusion pressure = MAP minus head height; in the upright position, for every 1 cm above the heart, MAP at the brain is ~0.77 mmHg less. Diabetics with cerebrovascular disease are particularly vulnerable
  • Maintain MAP ≥65–80 mmHg; consider measuring BP at the level of the external auditory meatus as a surrogate for cerebral perfusion

D. Cardiovascular Management

• Diabetics are at elevated ACC/AHA risk — have ECG and consider stress testing if multiple risk factors
• Increased incidence of silent myocardial ischaemia (autonomic neuropathy blunts pain perception)
• Consider initiating beta-blockers preoperatively if ≥2 cardiac risk factors (Barash p. 4062) — no evidence beta-blockers worsen glucose intolerance or mask hypoglycaemic symptoms
• Intraoperative ST-segment monitoring (V5 + II leads optimal)

E. Haemodynamic Lability

• Diabetic autonomic neuropathy impairs baroreceptor sensitivity and hypoxia-driven ventilatory drive
• Expect exaggerated hypotension at induction and haemodynamic swings during the case
• Use smaller, incremental induction doses; have vasopressors ready (phenylephrine preferred in beach chair to avoid excessive tachycardia from ephedrine)

F. Peripheral Neuropathy and Positioning

• Document all pre-existing neurological deficits before positioning
• Diabetics are more susceptible to peripheral nerve and pressure injuries — careful padding of all pressure points
• Vascular disease increases tissue ischaemia risk from compression

G. Renal Considerations

• Adjust drug doses for renal impairment (nephropathy common)
• Avoid nephrotoxic agents; cautious hydration

Monitoring Protocol

• Check blood glucose on arrival to the anaesthetic room
• Check every 1–2 hours intraoperatively (Barash p. 4086, 4098)
• For major/long surgery: consider continuous glucose monitoring (CGM) device — approved for hospital use since COVID-19 pandemic (Barash p. 2977)

Glucose Measurement Methods and Accuracy (Barash p. 2976)

Insulin Administration Strategy

• For short, non-invasive outpatient procedures in well-controlled diabetics: Subcutaneous sliding scale alone may suffice
• For longer or major surgery: IV regular insulin infusion is preferred over subcutaneous or long-acting insulin (Barash p. 4098)
  • Separate IV insulin infusion + separate IV glucose infusion (not combined GIK) — more easily adjusted
  • Insulin infusion via side-port of glucose infusion line (for safety)
  • A separate non-glucose isotonic solution (e.g., normal saline) is used for fluid replacement and loss compensation
• IV regular insulin (Barash Table 47-12): Onset 15 min, peak 15–30 min, duration 0.5–1 hour — ideal for titration
• Sliding scale insulin (RISS) as sole method is discouraged — leads to wide glucose fluctuations (Barash p. 2990)

Glucose Targets Intraoperatively

• Aim: 140–180 mg/dL (ADA/NICE-SUGAR-derived consensus)
• Avoid hypoglycaemia (glucose <70 mg/dL) — symptomatic sweating, tachycardia, confusion under GA may be masked
• Treat hypoglycaemia promptly with IV dextrose 50% (25 mL = 12.5 g glucose) or 10% dextrose infusion

Standard ASA/Routine Monitors

• ECG (5-lead if available; V5 + Lead II for optimal ischaemia detection)
• Pulse oximetry (SpO₂)
• Non-invasive blood pressure (NIBP) — consider invasive arterial line for:
  • Significant autonomic neuropathy
  • Established CAD or suspected silent ischaemia
  • Beach chair positioning with high risk of cerebral hypoperfusion
• Capnography (EtCO₂) — mandatory for GA with intubation
• Temperature monitoring — diabetics prone to hypothermia (peripheral vascular disease, autonomic neuropathy impairs thermoregulation)
• Peripheral nerve stimulator (TOF monitor) — for neuromuscular blockade monitoring (stiff joint syndrome → difficult airway; be sure of reversal before extubation)
• Depth of anaesthesia monitoring (BIS/Entropy) — particularly relevant in the sitting position where awareness risk may be higher

Specific Diabetic Monitoring

• Blood glucose: every 1–2 hours (Barash; Miller)
• Intraoperative urine output — diabetics have impaired renal autoregulation; maintain >0.5 mL/kg/hour
• Intra-arterial line — enables beat-to-beat BP measurement in beach chair position + frequent blood sampling for glucose

Postoperative Monitoring (PACU)

• Blood glucose on arrival to PACU and repeated every 1–2 hours
• Observe for hypoglycaemia — masked in post-anaesthesia recovery
• Watch for silent myocardial ischaemia — post-op ECG if concerned
• PONV prophylaxis (critical in Type 1 DM — early resumption of diet and insulin is essential) — use multimodal prophylaxis (dexamethasone + ondansetron ± scopolamine patch)

Induction

• Propofol or thiopental — no significant direct effect on glucose; propofol has mild anti-oxidant properties
• Consider modified RSI if gastroparesis/aspiration risk — preoxygenation, cricoid pressure, use of succinylcholine (if no contraindications) or high-dose rocuronium + sugammadex reversal plan
• Ketamine causes catecholamine release → hyperglycaemia; avoid or minimise in diabetics with poor glycaemic control

Maintenance

• Volatile anaesthetics (sevoflurane, desflurane): All potentiate peripheral glucose tolerance impairment to variable degrees; sevoflurane may have some cardioprotective preconditioning properties
• TIVA with propofol + remifentanil/fentanyl: Offers haemodynamic stability, less nausea, precise control — advantageous in diabetics
• Nitrous oxide: Can be used but increases PONV risk — problematic in gastroparetic diabetics; use judicious

Muscle Relaxation

• Rocuronium or vecuronium — standard; renal clearance of vecuronium is prolonged in significant nephropathy → prefer atracurium/cisatracurium (Hofmann elimination) if renal impairment
• Monitor NMB with TOF watch — critical; do not extubate without confirmed reversal (stiff joint → potential difficult re-intubation if airway lost)

Fluid Management

• Use balanced crystalloids (Hartmann's/PlasmaLyte) rather than saline if large volumes anticipated — saline → hyperchloraemic acidosis which can obscure DKA assessment
• Glucose-containing fluids only as part of glucose management protocol — not as routine IV fluid
• Avoid dextrose infusions in euglycaemic patients (risk of hyperglycaemia)

1. Resume oral intake as early as possible → allows transition back to oral glucose-lowering regimen
2. Glucose monitoring continues in PACU and ward — 4-hourly on ward for stable patient; every 1–2 hours if labile
3. PONV prophylaxis with multimodal agents — PONV in a Type 1 diabetic delays oral intake and insulin resumption, risking DKA
4. Wound healing: Diabetics have impaired neutrophil function, reactive oxygen species overproduction, and vascular disease → increased infection risk; strict asepsis, glycaemic control
5. Restart medications: Oral agents resumed once patient is eating. Metformin is restarted only once renal function is confirmed adequate. SGLT-2 inhibitors can be restarted after wound has healed and patient is eating normally.
6. Consider multimodal analgesia — regional nerve blocks reduce stress response (↓ cortisol, catecholamines → less hyperglycaemia); NSAIDs with caution in diabetic nephropathy; paracetamol safe
7. Interscalene block (ISB) as part of shoulder surgery anaesthesia: If used as an adjunct or sole technique, monitor for autonomic effects (Horner syndrome, phrenic nerve palsy) — particularly important since diabetics may already have compromised respiratory reserve

SECTION C — SCENARIO 2: 30-YEAR-OLD DIABETIC FOR LSCS (LOWER SEGMENT CAESAREAN SECTION)

1. Pre-existing Type 1 DM — absolute insulin deficiency; autoimmune
2. Pre-existing Type 2 DM — insulin resistance ± secretory defect; often obesity-related
3. Gestational Diabetes Mellitus (GDM) — diabetes first diagnosed during second or third trimester; the most common form in pregnancy; usually resolves postpartum but increases lifetime risk of Type 2 DM
4. Secondary diabetes — steroid-induced (e.g., betamethasone given for fetal lung maturity), pancreatic disease

• 1-hour 50g glucose challenge test (GCT): if ≥140 mg/dL → 3-hour 100g OGTT for confirmation
• Or: Fasting glucose ≥92 mg/dL, 1-hour ≥180, 2-hour ≥153 on 75g OGTT (IADPSG criteria)
• Risk factors: Age >25, obesity, family history of DM, prior macrosomic baby, polycystic ovary syndrome

• Pre-existing DM carries higher risk of established end-organ disease (neuropathy, nephropathy, retinopathy, CAD)
• GDM typically has fewer end-organ complications but introduces:
  • Macrosomia (fetal overgrowth) → obstructed labour → LSCS
  • Pre-eclampsia and hypertension risk
  • Neonatal hypoglycaemia (neonatal team must be present)
  • Polyhydramnios → aspiration risk

• Placental hormones (HPL, progesterone, cortisol, prolactin) → peripheral insulin resistance
• Insulin requirements rise progressively through pregnancy (especially in the 2nd–3rd trimester)
• Impaired fasting glucose is normal in pregnancy due to increased peripheral glucose uptake by fetus and placenta

History

• Urgency of LSCS (Category I–IV): Urgency governs the choice between spinal, epidural, and GA
• Type of diabetes, duration, current glycaemic control
• Current medications: Insulin type and doses; metformin (last dose?); SGLT-2 inhibitors (if any — must have been discontinued 3–4 days before); GLP-1 agonists (aspiration risk)
• Obstetric history: Gestational age; antenatal complications; fetal well-being; placenta position
• Pre-eclampsia (complicates 15–20% of diabetic pregnancies) → affects anaesthetic choice (thrombocytopenia → contraindication to regional block?)

Systematic Review for End-Organ Disease

• Cardiovascular: Silent ischaemia, hypertension (superimposed pre-eclampsia in DM patients)
• Renal: Diabetic nephropathy + pre-eclampsia (superimposed) — check proteinuria, creatinine
• Neurological: Peripheral neuropathy → document before regional block
• Airway: Stiff joint syndrome (longstanding T1DM) + pregnancy-related oropharyngeal oedema → combined difficult airway

Laboratory Investigations

• Blood glucose on arrival and 1-hourly (more frequently if unwell)
• HbA1c
• FBC — platelet count (pre-eclampsia → thrombocytopenia; minimum platelet count for neuraxial block: 70,000–100,000/mm³ depending on institutional policy)
• Coagulation (PT, APTT) if pre-eclampsia or on LMWH
• Renal function (creatinine, uric acid — uric acid elevated in pre-eclampsia)
• LFTs (HELLP syndrome screen if severe pre-eclampsia)
• Group and screen / crossmatch (obstetric haemorrhage risk)
• ECG (if pre-existing DM with cardiac risk factors)

Preferred Technique: SPINAL ANAESTHESIA

1. Avoids the risks of GA in a potentially difficult airway (pregnancy + diabetic stiff joint syndrome)
2. Avoids aspiration risk — these patients are "full stomach" even after fasting (gastric stasis from autonomic neuropathy)
3. Lower stress response vs. GA → better glycaemic control (less catecholamine/cortisol surge)
4. Neonatal benefits — avoids foetal exposure to GA agents
5. Superior postoperative analgesia — intrathecal opioids (morphine 100–200 µg, fentanyl 10–25 µg) provide prolonged analgesia
6. Conscious patient — facilitates immediate maternal–neonatal bonding

• Heavy bupivacaine 0.5%: 1.5–2.0 mL (typically 10–12 mg)
• Intrathecal fentanyl 10–25 µg — onset analgesia
• Intrathecal morphine 100–200 µg — prolonged postoperative analgesia (4–18 hours)
• Block level required: T4 (nipple line) for complete LSCS anaesthesia

When Epidural is Preferred

• If labour epidural is already in-situ → epidural top-up for LSCS
• Non-urgent LSCS where gradual onset of block is preferred
• Allows titration in haemodynamically unstable patients

When Combined Spinal-Epidural (CSE) is Used

• Ultra-low-dose spinal supplemented by epidural if surgery is prolonged
• Allows top-up if spinal inadequate without repeat spinal

When GA is Required

• Category I (crash) LSCS when there is no time for neuraxial block
• Contraindications to neuraxial block: Thrombocytopenia (<70,000), coagulopathy, patient refusal, raised ICP, local infection, severe uncorrected hypovolaemia
• Failed or inadequate spinal/epidural

• Pregnancy alone: failed intubation rate ~1:300 (vs. 1:2,000 in general surgery)
• Diabetic stiff joint syndrome compounds this → among the highest-risk airways in anaesthesia
• Must have:
  • Fibreoptic laryngoscope + video laryngoscope immediately available
  • Declare difficult airway before induction
  • Consider awake fibreoptic intubation if airway exam is very concerning
  • Follow DAS (Difficult Airway Society) obstetric failed intubation algorithm

• Highest-risk scenario: diabetic gastroparesis + pregnant (↓ LOS tone, ↑ gastric pressure)
• Rapid Sequence Induction (RSI) is mandatory for GA in all obstetric patients
• Preoxygenation (100% O₂ for ≥3 minutes or 8 vital capacity breaths)
• Cricoid pressure (Sellick manoeuvre) applied until intubation confirmed
• IV sodium citrate 30 mL (oral) given ≤30 min before induction (neutralises gastric acid)
• IV ranitidine 150 mg or pantoprazole the night before and morning of LSCS
• IV metoclopramide 10 mg — prokinetic; promotes gastric emptying, reduces aspiration risk; also important as antiemetic

• RSI with induction doses followed by volatile agent; thiopental (5–7 mg/kg) or propofol (2–2.5 mg/kg) as induction agent
• Use of BIS monitoring to detect awareness

• All GA agents cross the placenta → neonatal sedation/respiratory depression
• Minimise the induction-delivery (I-D) interval — ideally <8 minutes
• Neonatal resuscitation team must be present in room

• Physiological response to laryngoscopy + intubation (catecholamine surge) → acute hyperglycaemia
• Stress hormones from surgery (cortisol, glucagon, catecholamines) → perioperative hyperglycaemia
• Monitor glucose from arrival; use IV insulin protocol

1. Autonomic neuropathy → impaired compensatory baroreceptor reflexes → deeper and more prolonged hypotension
2. Pre-existing hypertension (common in DM) → acute BP drop may cause more profound organ hypoperfusion
3. Uteroplacental insufficiency → foetal distress if uterine blood flow drops

• Left uterine displacement (15°) — relieves aortocaval compression
• Preloading or co-loading with crystalloid (1 litre of Hartmann's rapidly given before or during spinal injection)
• Colloid co-load is more effective than crystalloid preload for maintaining BP
• Vasopressors:
  • Phenylephrine (alpha-agonist): Now the first-line vasopressor for spinal hypotension in obstetrics — maintains maternal BP and uteroplacental blood flow, prevents reflex tachycardia. Particularly advantageous in diabetics with autonomic neuropathy (already have resting tachycardia — phenylephrine does not add to it)
  • Ephedrine (mixed alpha + beta): Previously first-line; now second-line. Stimulates beta-receptors → crosses placenta → may cause fetal tachycardia and acidosis; stimulates glucogenolysis → hyperglycaemia in the diabetic
  • Noradrenaline (norepinephrine): Emerging data support use; may be better than phenylephrine in patients with underlying bradycardia
• Prophylactic vasopressor infusion: Phenylephrine infusion (50–100 µg/min) from the moment of spinal injection is now standard in many obstetric units

Preoperative

• Check blood glucose on arrival (ideally fasting 4–6 hours before elective LSCS)
• Target glucose: 70–140 mg/dL for the parturient (tighter than non-pregnant surgical patients to prevent neonatal hypoglycaemia — a neonate exposed to maternal hyperglycaemia secretes excess insulin and becomes hypoglycaemic after delivery)
• Schedule LSCS as first case — minimise fasting duration
• Type 1 DM: Give half to two-thirds of usual intermediate insulin subcutaneously on the morning of surgery (never omit all insulin entirely)
• Type 2 DM on OHAs: Withhold all oral agents; manage with insulin infusion
• If blood glucose >140 mg/dL → start IV regular insulin infusion before proceeding

Intraoperative

• Monitor blood glucose every 30–60 minutes (more frequent than for non-obstetric cases — neonatal hypoglycaemia is the key concern)
• Maintain glucose 70–140 mg/dL throughout
• Run 5% dextrose at 100 mL/hour as a background infusion with a separate insulin infusion titrated to glucose
• Avoid glucose boluses (rapid glucose elevation → neonatal hyperinsulinism → neonatal hypoglycaemia after cord clamping)
• Lactated Ringer's (Hartmann's) solution for volume replacement (contains 28 mmol/L lactate which does not cause clinically significant hyperglycaemia)

Post-Delivery

• After placental delivery: insulin requirements drop dramatically (placental diabetogenic hormones removed)
• Risk of hypoglycaemia is highest in the immediate post-delivery period
• Reduce insulin infusion after cord clamping
• Monitor glucose every 1–2 hours in PACU and postoperative ward

Neonatal Team

• Neonatal hypoglycaemia is common (especially macrosomic infants of poorly controlled DM mothers)
• Neonatal resuscitation team must be present in the delivery room
• Early breastfeeding + glucose monitoring of the neonate

Maternal Monitoring

Foetal/Neonatal Monitoring

• Intraoperative FHR (foetal heart rate) monitoring if available
• APGAR scores at 1 and 5 minutes
• Neonatal blood glucose within 30 minutes of birth and serially thereafter

Multimodal Analgesia Approach

• Provides 4–18 hours of excellent postoperative analgesia
• Reduces opioid requirements → less sedation, earlier mobilisation, earlier breastfeeding
• Side effects: pruritus (treat with naloxone 0.04 mg IV or ondansetron), nausea/vomiting, delayed respiratory depression (risk up to 18 hours — observe regularly)
• Requires 12–24 hours of regular respiratory monitoring

• Highly effective multimodal component
• Caution in diabetic nephropathy — NSAIDs are relatively contraindicated (nephrotoxic); use paracetamol and tramadol instead if eGFR is impaired

• Bilateral TAP blocks at the end of LSCS provide somatic analgesia to the abdominal wall
• Particularly useful as an adjunct or if intrathecal morphine was not given
• Reduces postoperative morphine requirements

• Critical in the diabetic parturient — nausea and vomiting delay resumption of oral intake and insulin
• Ondansetron 4 mg IV; dexamethasone 4–8 mg IV (note: dexamethasone causes hyperglycaemia — monitor glucose carefully and cover with insulin); transdermal scopolamine patch

KEY TABLES

Insulin Pharmacology (Barash Table 47-12)

Perioperative Glucose Targets Summary

Diabetic Complications Checklist for Preoperative Assessment