DM - etiopathology , signs and symptoms Pre-op evaluation & optimisation with management of uncontrolled DM posted for OT Major complications of DM with DKA in full detail MD Anaesthesia pg exam answer

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DIABETES MELLITUS - MD Anaesthesia PG Exam Answer

PART 1: DIABETES MELLITUS - ETIOPATHOLOGY, SIGNS AND SYMPTOMS

Definition and Classification

Diabetes mellitus (DM) is a group of metabolic disorders characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The major types are:

Type 1 DM (T1D) - autoimmune destruction of beta cells, absolute insulin deficiency
Type 2 DM (T2D) - insulin resistance + relative beta-cell insufficiency
MODY (Maturity Onset Diabetes of the Young) - monogenic, single-gene beta-cell dysfunction
Gestational DM
Secondary DM - Cushing's, acromegaly, pancreatitis, drug-induced (steroids, thiazides)

Etiopathology

Type 1 DM - Autoimmune Mechanism

T1D is an autoimmune disease characterized by progressive destruction of islet beta cells, leading to absolute insulin deficiency. The pathogenesis involves:

Genetic susceptibility - HLA-DR3, HLA-DR4 alleles strongly associated; also HLA-DQ loci
Failure of self-tolerance in T cells - autoreactive CD4+ and CD8+ T lymphocytes target islet antigens
Autoantibodies - circulating autoantibodies to:
- Islet cell antigens (ICA)
- Insulin (IAA)
- Glutamic acid decarboxylase (GAD65)
- Tyrosine phosphatase IA-2 and IA-2β
- Zinc transporter 8 (ZnT8)
Insulitis - lymphocytic infiltration of islets, leading to progressive beta-cell destruction
Environmental triggers - viral infections (Coxsackievirus B4, enterovirus), early diet (cow's milk proteins), gut microbiome alterations

(Robbins, Cotran & Kumar Pathologic Basis of Disease)

Type 2 DM - Metabolic Mechanism

T2D has no autoimmune basis. Its central pathogenic features are:

A. Insulin Resistance - the primary defect in most patients:

Obesity contributes via excess free fatty acids (FFAs), adipocytokines (resistin, TNF-alpha), and chronic low-grade inflammation
Impaired post-receptor signaling (IRS-1/PI3K pathway defect)
Ectopic fat deposition in liver and muscle worsens peripheral resistance
"Lipotoxicity" and "glucotoxicity" compound the defect over time

B. Beta-Cell Dysfunction - relative insulin deficiency:

Progressive decline in beta-cell mass and function
Amyloid deposition in islets (islet amyloid polypeptide, IAPP)
Impaired first-phase insulin secretion - earliest detectable defect
As disease progresses, second-phase secretion also fails

Incretin defect - reduced GLP-1 and GIP effect also contributes to insufficient insulin response.

Mechanisms of Hyperglycemia-Induced Tissue Damage (Common to Both Types)

Four pathways link sustained hyperglycemia to long-term complications:

Advanced Glycation End-products (AGEs) - non-enzymatic glycosylation of proteins/lipids, cross-linking collagen, impairing vascular function
Protein Kinase C (PKC) activation - triggered by intracellular diacylglycerol accumulation, alters vascular permeability and growth factor signaling
Polyol pathway - glucose converted to sorbitol (aldose reductase), osmotic cell damage; seen in lens (cataracts), peripheral nerves
Hexosamine pathway overload - excess glucose flux, impairs insulin signaling

(Robbins, Cotran & Kumar; Harrison's 22nd Ed.)

Signs and Symptoms

Classical Osmotic Symptoms ("3 Polys + Weight Loss")

Symptom	Mechanism
Polyuria	Osmotic diuresis from glucosuria (glucose exceeds renal threshold ~180 mg/dL)
Polydipsia	Hyperosmolality stimulates thirst center
Polyphagia	Cellular starvation despite hyperglycemia; insulin deficiency prevents glucose uptake
Weight loss	Catabolism of fat and protein; prominent in T1D

Type 1 DM - Presentation

Acute onset, younger patients (though any age)
Weeks of polyuria/polydipsia, fatigue, weight loss
May present acutely with Diabetic Ketoacidosis (DKA)
Thin habitus; no acanthosis nigricans

Type 2 DM - Presentation

Often asymptomatic for years - diagnosed incidentally
Insidious onset, middle-aged/elderly, often obese
May present with complications already established at diagnosis:
- Blurred vision (osmotic lens swelling)
- Recurrent skin infections (furuncles, candidiasis)
- Delayed wound healing
- Nocturia
Acanthosis nigricans (insulin resistance marker in skin folds, neck)
Signs of metabolic syndrome (central obesity, hypertension, dyslipidemia)

Diagnostic Criteria (ADA)

Test	Diabetic	Pre-diabetic
Fasting plasma glucose	≥ 126 mg/dL	100-125 mg/dL
2-hr OGTT	≥ 200 mg/dL	140-199 mg/dL
Random glucose + symptoms	≥ 200 mg/dL	-
HbA1c	≥ 6.5%	5.7-6.4%

PART 2: PREOPERATIVE EVALUATION AND OPTIMIZATION OF UNCONTROLLED DM FOR OT

Why DM Matters for Anaesthesia

Diabetic patients presenting for surgery carry significant risks:

Increased infection / impaired wound healing
Autonomic neuropathy (cardiovascular instability, silent MI, gastroparesis)
Difficult airway (limited joint mobility, stiff joint syndrome, glycosylation of cervical ligaments)
Renal impairment (contrast nephropathy, fluid management)
Risk of perioperative hyperglycemia and hypoglycemia
Silent myocardial ischemia

Pre-operative Assessment

History:

Type of DM (T1 vs T2), duration, current treatment (OHAs / insulin type and dose)
Level of glycemic control - recent HbA1c, home glucose readings
Insulin:carbohydrate ratio and correction factor (for T1D)
Last dose of any medications (especially long-acting insulin, metformin, SGLT2 inhibitors)
History of hypoglycemic episodes - frequency, awareness, nocturnal episodes
End-organ evaluation (see below)

Assessment of End-Organ Complications:

System	Assessment
Cardiovascular	Resting ECG (silent MI, LBBB), exercise tolerance, echo if suspected dysfunction; autonomic neuropathy - postural BP, resting HR > 100 bpm
Renal	Serum creatinine, eGFR, urine albumin/creatinine ratio; nephropathy affects fluid and drug management
Neuropathy	Peripheral neuropathy, autonomic dysfunction (orthostatic hypotension, impaired HR variability, risk of aspiration due to gastroparesis)
Retinopathy	Ophthalmology review, positioning care (avoid prone if severe)
Airway	Prayer sign (limited joint mobility, "steeple sign"), reduced neck mobility; can predict difficult laryngoscopy

Laboratory Investigations:

FBS, PPBS, HbA1c (reflects 3-month control)
CBC, renal function tests (BUN, creatinine, electrolytes)
Liver function tests
ECG, chest X-ray
Urine routine (ketones, protein, infection)
Coagulation profile if planned regional anaesthesia

Optimization of Uncontrolled DM Before Elective Surgery

Target: HbA1c < 8-9% for elective surgery (ADA); fasting glucose 140-180 mg/dL perioperatively.

"Elective surgeries should be delayed in patients with poor glycemic control until optimization or a sustainable plan is in place." - Barash Clinical Anesthesia, 9th Ed.

Specific Interventions:

Optimize glycemic control - intensify insulin regimen; refer to endocrinology if needed
Treat infections - source of uncontrolled hyperglycemia must be identified and treated
Correct electrolytes - hypokalemia, hyponatremia, dehydration
Stop nephrotoxic agents - metformin should be held 24-48 hrs before major surgery (risk of lactic acidosis if renal hypoperfusion); SGLT2 inhibitors stopped 3-7 days preop (risk of euglycemic DKA perioperatively; SGLT2 inhibitor effect may persist 10-14 days)
Optimize blood pressure - ACE inhibitors/ARBs - hold on day of surgery (hypotension risk)
Cardiac optimization - beta-blockers if IHD; revascularization if significant CAD before elective major surgery

Perioperative Insulin Management Protocol

Scheduling:

Diabetic patients should be scheduled as FIRST CASE on the operating list (minimizes fasting duration and metabolic disruption)
Minimize prolonged fasting (overnight fast maximum 8-12 hrs)

Day Before Surgery:

Continue usual insulin regimen
Hold sulfonylureas, SGLT2 inhibitors, metformin

Morning of Surgery:

Agent	Action
Long-acting insulin (basal)	Give 75-80% of usual dose the evening before / morning of surgery
Short-acting / mealtime insulin	Omit on morning of surgery (no food = no mealtime dose)
Metformin	Hold 24-48 hrs preop (especially major surgery)
SGLT2 inhibitors	Hold 3-7 days preop
GLP-1 agonists	Hold day before surgery (delayed gastric emptying concern; increased aspiration risk)
Sulfonylureas	Hold morning of surgery (hypoglycemia risk)

Intraoperative Target:

Blood glucose: 140-180 mg/dL (hyperglycemia worsens outcomes; hypoglycemia is dangerous under GA where symptoms masked)
Monitor glucose every 1-2 hours intraoperatively

Variable Rate Intravenous Insulin Infusion (VRIII) / GKI Infusion:

Used for major surgery, T1D, uncontrolled T2D
GKI (Glucose-Potassium-Insulin) regimen: 5% dextrose + KCl + regular insulin in same bag
VRIII (sliding scale): Separate insulin infusion titrated to hourly glucose targets
Target glucose 6-10 mmol/L (108-180 mg/dL) during surgery

Gastroparesis / Aspiration Risk:

DM autonomic neuropathy - gastric emptying delayed
Use rapid sequence induction (RSI) with cricoid pressure if gastric stasis suspected
Consider metoclopramide, H2 antagonist preoperatively

Postoperatively:

Resume oral intake and baseline insulin regimen as soon as possible
PONV prophylaxis essential (promotes early resumption of oral intake and insulin regimen)
Continue glucose monitoring 2-4 hourly until stable

PART 3: MAJOR COMPLICATIONS OF DM

CHRONIC COMPLICATIONS

These are classified into Microvascular and Macrovascular complications. All arise from sustained hyperglycemia-induced damage via the four mechanisms detailed above.

A. Microvascular Complications

1. Diabetic Retinopathy

DM is the leading cause of new blindness in adults aged 20-74 years.

Pathogenesis:

Loss of retinal pericytes, increased vascular permeability
Basement membrane thickening, capillary microaneurysms
Alterations in retinal blood flow, retinal ischemia

Stages:

Non-Proliferative Diabetic Retinopathy (NPDR):

Appears late in first decade / early second decade of hyperglycemia
Retinal vascular microaneurysms, blot hemorrhages, cotton-wool spots
More severe NPDR: venous caliber changes, intraretinal microvascular abnormalities (IRMA)

Proliferative Diabetic Retinopathy (PDR):

Hallmark: neovascularization in response to retinal hypoxia (VEGF-driven)
New vessels near optic nerve / macula rupture easily
Leads to: vitreous hemorrhage, fibrosis, traction retinal detachment
Clinically significant macular edema can occur at any stage

Risk factors: Duration of DM, degree of glycemic control, hypertension, nephropathy, dyslipidemia.

Treatment:

Intensive glycemic and BP control (delays progression)
Panretinal laser photocoagulation for PDR
Anti-VEGF (intravitreal bevacizumab/ranibizumab) for macular edema

(Harrison's 22nd Ed.)

2. Diabetic Nephropathy

Leading cause of CKD and ESRD requiring renal replacement therapy.

Affects 20-40% of diabetic patients. Associated with markedly increased cardiovascular mortality.

Pathogenesis:

Chronic hyperglycemia activates soluble factors (angiotensin II, endothelin, growth factors, AGEs)
Hemodynamic changes: glomerular hyperfiltration/hyperperfusion, increased intraglomerular pressure
Structural changes: GBM thickening, mesangial expansion (Kimmelstiel-Wilson nodules - pathognomonic), glomerulosclerosis
Epigenetic changes, tubulointerstitial fibrosis

Natural History (Mogensen's Stages):

Stage	Feature	GFR	Albumin
I - Hyperfiltration	Glomerular hyperperfusion	Increased	Normal
II - Silent	GBM thickening, mesangial expansion	Normal/high	Normal
III - Incipient (Microalbuminuria)	Early nephropathy	Slightly reduced	30-299 mg/g
IV - Overt (Macroalbuminuria)	Clinical nephropathy	Declining	>300 mg/g
V - ESRD		<15 mL/min	Heavy proteinuria

Screening: Annual UACR (spot urine) and eGFR:

Start screening from 5 years after T1D onset
At time of diagnosis for T2D

Treatment:

Glycemic control (target HbA1c < 7%)
BP control: ACEI or ARB (first-line; reduces intraglomerular pressure and proteinuria)
SGLT2 inhibitors (empagliflozin, dapagliflozin) - renoprotective independent of glucose effect
GLP-1 agonists (liraglutide, semaglutide) - reduce composite renal outcomes

(Harrison's 22nd Ed.)

3. Diabetic Neuropathy

Most common complication affecting up to 50% of patients over time.

Types:

Type	Features
Distal symmetric polyneuropathy	Most common; length-dependent sensorimotor; "glove-and-stocking" loss; starts with loss of vibration and temperature sensation; can progress to loss of pain, deep tendon reflexes
Autonomic neuropathy	Cardiovascular (resting tachycardia, orthostatic hypotension, silent MI), GI (gastroparesis, constipation/diarrhea), genitourinary (neurogenic bladder, erectile dysfunction), sudomotor dysfunction
Focal/Multifocal neuropathy	Cranial nerve palsies (III, VI), diabetic amyotrophy (lumbosacral plexopathy), thoracoabdominal radiculopathy
Charcot neuroarthropathy	Neuropathic osteoarthropathy of foot/ankle

Pathogenesis: Polyol pathway (sorbitol accumulation), reduced nerve conduction, endoneurial ischemia, oxidative stress.

Anaesthetic implications of autonomic neuropathy:

Hemodynamic instability under anaesthesia (blunted compensatory responses)
Aspiration risk (gastroparesis)
Perioperative silent MI (absent angina)
Temperature dysregulation

B. Macrovascular Complications

The dominant cause of morbidity and mortality in T2D.

Complication	Notes
Coronary Artery Disease (CAD)	2-4x increased risk; often silent (no chest pain due to neuropathy); DM considered CAD equivalent
Cerebrovascular disease (stroke)	2x increased risk; particularly lacunar infarcts
Peripheral Arterial Disease (PAD)	Claudication, rest pain, critical limb ischemia, diabetic foot ulcers, gangrene
Hypertension	Present in ~75% of T2D patients; major driver of CVD and nephropathy
Dyslipidemia	Characteristic pattern: high TG, low HDL, small dense LDL particles

Pathogenesis: Chronic hyperglycemia and insulin resistance accelerate atherosclerosis via:

Endothelial dysfunction (reduced NO, increased oxidative stress)
Foam cell formation, lipid deposition
Increased platelet aggregation
AGE-mediated collagen crosslinking and arterial stiffening

C. Other Complications

Complication	Notes
Diabetic foot	Neuropathy + PAD + infection triad; leading cause of non-traumatic lower limb amputation
Infections	Impaired neutrophil function, mucocutaneous candidiasis, recurrent UTIs, rhinocerebral mucormycosis, necrotizing fasciitis, malignant otitis externa
Skin	Necrobiosis lipoidica, diabetic dermopathy, bullosis diabeticorum, acanthosis nigricans

DIABETIC KETOACIDOSIS (DKA) - IN FULL DETAIL

Definition

DKA is an acute, life-threatening metabolic emergency characterized by the triad of:

Hyperglycemia (glucose usually > 250 mg/dL)
Metabolic ketoacidosis (pH < 7.3; HCO3 < 15 mmol/L; increased anion gap)
Ketonemia / ketonuria

Primarily occurs in Type 1 DM, but can occur in T2D under stress.

Pathophysiology of DKA

Precipitating causes (the "6 I's"):

Infection (most common - pneumonia, UTI, gastroenteritis, sepsis)
Insulin omission / non-compliance (missed doses)
Infarction (MI, stroke, mesenteric ischemia)
Intoxication (cocaine, alcohol)
Iatrogenic (steroids, SGLT2 inhibitors - euglycemic DKA)
Initial presentation (new diagnosis T1D)
Also: pancreatitis, trauma, pregnancy

Biochemical cascade:

Absolute insulin deficiency + stress hormone excess (glucagon, cortisol, catecholamines, GH) →

Unrestrained gluconeogenesis and glycogenolysis → severe hyperglycemia
Impaired peripheral glucose uptake (no insulin) → hyperglycemia worsens
Lipolysis → massive release of free fatty acids → hepatic ketogenesis
Three ketone bodies formed:
- Acetone (volatile, "fruity breath")
- Beta-hydroxybutyrate (~80% of serum ketones in DKA)
- Acetoacetic acid (~20%)
Anion gap metabolic acidosis (accumulation of beta-hydroxybutyrate and acetoacetate)
Osmotic diuresis from glucosuria → profound dehydration, electrolyte loss
Total body potassium depletion (deficit 3-5 mEq/kg) from osmotic diuresis and vomiting

Key electrolyte paradox:

Serum K+ may be normal or elevated at presentation (acidosis drives K+ out of cells)
Total body K+ is severely depleted
With insulin + fluid treatment, K+ rapidly shifts intracellularly → profound hypokalemia if not replaced

Clinical Features of DKA

(Harrison's 22nd Ed., Table 16-8)

Symptoms:

Nausea and vomiting
Thirst and polyuria (early)
Abdominal pain (may mimic acute abdomen / pancreatitis)
Shortness of breath

Physical Findings:

Tachycardia
Dehydration (dry mucous membranes, poor skin turgor, sunken eyes)
Hypotension (in severe DKA)
Kussmaul respirations - deep, rapid, sighing breathing (respiratory compensation for metabolic acidosis)
Fruity / acetone breath (volatile acetone)
Abdominal tenderness (may simulate surgical abdomen)
Lethargy, obtundation, coma (severe; due to hyperosmolality and acidosis)
Cerebral edema - rare but most feared complication, especially in children

Laboratory Findings in DKA

Parameter	Finding
Blood glucose	> 250 mg/dL (usually 350-500; rarely > 800)
Arterial pH	< 7.30
Serum HCO3	< 15 mmol/L
Anion gap	Elevated (>12 mEq/L) - anion gap = Na - (Cl + HCO3)
Beta-hydroxybutyrate	Elevated (best diagnostic marker)
Urine ketones	Strongly positive
Serum K+	Normal or elevated (but total body depleted)
Serum Na+	Often low (dilutional; also pseudohyponatremia from lipemia)
BUN/Creatinine	Elevated (prerenal azotemia)
Amylase/Lipase	Often elevated (even without pancreatitis)
WBC	Elevated with left shift (even without infection - stress response)
Osmolality	Elevated

Note on ketone measurement: The nitroprusside test (urine dipstick) detects acetoacetate and acetone but is relatively insensitive to beta-hydroxybutyrate. In early DKA treatment, apparent increase in detected ketones may occur as beta-hydroxybutyrate converts to acetoacetate - this is not clinical worsening.

Severity Classification of DKA

Severity	pH	HCO3 (mmol/L)	Mental Status
Mild	7.25 - 7.30	15-18	Normal/alert
Moderate	7.00 - 7.25	10-15	Mildly obtunded
Severe	< 7.00	< 10	Stupor / coma

Management of DKA (Harrison's 22nd Ed. + Barash Clinical Anesthesia 9th Ed.)

Step-by-step Protocol:

1. Initial Assessment and Monitoring:

Confirm diagnosis: beta-hydroxybutyrate, blood glucose, ABG/VBG
Vital signs, GCS, urine output
Identify precipitant: cultures, CXR, ECG, pregnancy test
Insert NG tube if vomiting or altered consciousness (aspiration prevention)
Foley catheter (urine output monitoring)

2. Fluid Resuscitation (FIRST and most important step):

0.9% Normal Saline or Lactated Ringer's: 2-3 L over first 1-3 hours (10-20 mL/kg/hr)
Then 0.45% saline or Ringer's Lactate at 250-500 mL/hr (correct remaining deficit over 24 hrs)
Total fluid deficit: 3-5 L typically (can be up to 10 L in severe cases)
Switch to 5-10% dextrose + 0.45% saline when glucose falls to 250 mg/dL (continue insulin but add dextrose to prevent hypoglycemia)
Note: Ringer's Lactate associated with faster DKA resolution and less hyperchloremia vs. normal saline

3. Insulin Therapy:

Do NOT start insulin if K+ < 3.3 mmol/L - correct potassium first
IV Regular Insulin: bolus 0.1 units/kg, then continuous infusion at 0.1 units/kg/hr
If blood glucose does not fall by 10% in first hour: give additional bolus 0.1 units/kg
Target glucose fall: 50-70 mg/dL per hour
When glucose < 250 mg/dL: reduce insulin infusion to 0.02-0.1 units/kg/hr, add dextrose
For mild-moderate DKA: subcutaneous rapid-acting insulin analogues can be used (0.1 units/kg q1h or 0.2 units/kg q2h)

4. Potassium Replacement (critical):

Serum K+	Action
< 3.3 mmol/L	Give 20-40 mEq/hr IV, hold insulin until K+ > 3.3
3.5-5.0 mmol/L	Add 20-30 mEq to each litre IV fluid
> 5.0 mmol/L	Start insulin but hold K+ replacement; recheck K+ every 2 hours

Continuous ECG monitoring when K+ replacement rate > 10 mEq/hr.

5. Bicarbonate:

Routine use NOT recommended (multiple studies show no benefit in resolution time or outcome)
Consider only if:
- pH < 6.9 even without hemodynamic instability
- Hemodynamically unstable with pH < 7.1
- Life-threatening hyperkalemia
Give 50-100 mmol NaHCO3 in 200 mL sterile water + 10 mEq KCl over 1 hour if used

6. Phosphate:

Hypophosphatemia occurs with acidosis correction
If severe (< 1 mg/dL) or causing ventilatory muscle weakness: replace with potassium phosphate

7. Monitoring and Resolution Criteria:

Blood glucose: every 1-2 hours
Electrolytes, anion gap, pH, HCO3: every 2-4 hours for first 24 hours
Vital signs, mental status, urine output: every 1-4 hours

Resolution criteria (all must be met):

Blood glucose < 200-250 mg/dL
Serum HCO3 ≥ 18 mmol/L
Venous pH > 7.3
Anion gap normalized
Mental status normal

8. Transition to Subcutaneous Insulin:

Begin long-acting insulin as soon as patient is eating
Allow 2-4 hour overlap between subcutaneous and IV insulin infusion before stopping infusion (prevents rebound DKA)
Do not stop IV insulin just because glucose is < 250 - ketosis may persist

Complications of DKA (and its Treatment)

Complication	Notes
Cerebral edema	Most dangerous; primarily in children; caused by rapid fluid shifts; presents with deteriorating GCS after initial improvement; treat with mannitol / hypertonic saline
Hypokalemia	From insulin and fluid therapy; can cause cardiac arrhythmias, respiratory muscle weakness
Hypoglycemia	From excessive insulin without dextrose supplementation
Aspiration pneumonia	Gastroparesis + vomiting + altered consciousness
Venous thromboembolism	Hypercoagulable state from dehydration; DVT/PE
Acute respiratory distress syndrome (ARDS)	Rare; from aggressive fluid resuscitation
Hypophosphatemia	Ventilatory failure, hemolysis, rhabdomyolysis
Upper GI bleeding	Acute gastric erosions
Hyperchloremic metabolic acidosis	After treatment with large volumes of normal saline (use LR preferentially)

DKA vs. Hyperosmolar Hyperglycaemic State (HHS) - Key Distinctions

Feature	DKA	HHS
DM type	T1D (mainly)	T2D (mainly)
Glucose	250-600 mg/dL	≥ 600 mg/dL (often > 1000)
pH	< 7.30	Usually normal (> 7.30)
HCO3	< 15 mmol/L	Normal (> 20)
Ketones	Strongly positive	Absent or trace
Osmolality	Mildly elevated	> 330 mOsm/L
Mental status	Variable	Profound obtundation
Mortality	~1-5%	~10-20% (higher)

Anaesthesia-Specific Points for DKA

Active DKA is an absolute contraindication to elective surgery
Emergency surgery in DKA: simultaneous resuscitation and surgery with intensivist-anaesthesiologist collaboration
RSI mandatory (full stomach from gastroparesis, vomiting)
Volatile anaesthetics and opioids do not alter insulin secretion significantly, but surgical stress greatly worsens hyperglycemia
SGLT2 inhibitor-associated euglycemic DKA: glucose may be near-normal (250-300 mg/dL) making diagnosis easy to miss; stop SGLT2 inhibitors 3-7 days preoperatively
Relapse of SGLT2 inhibitor-associated DKA is common if nutritional intake has not been re-established (pharmacologic effect persists 10-14 days after stopping)

References: Barash, Cullen & Stoelting's Clinical Anaesthesia 9th Ed. | Harrison's Principles of Internal Medicine 22nd Ed. (2025) | Robbins, Cotran & Kumar Pathologic Basis of Disease | Quick Compendium of Clinical Pathology 5th Ed. | Tietz Textbook of Laboratory Medicine 7th Ed.

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