Free exam prep

CAMC Regional Medical Registration Examination Part 1

Practice Questions100 questions Study Guide64 topics

4.1 Diabetes Mellitus, Diabetic Ketoacidosis & Hyperosmolar Hyperglycaemic State

Q: A 19-year-old man with Type 1 diabetes is brought to the emergency department after 2 days of vomiting, polyuria, and progressive breathlessness. On physical examination, he appears severely dehydrated with dry mucous membranes and deep, rapid breathing. Vital signs: BP 96/60 mmHg, HR 122 bpm, RR 30 breaths/min, SpO2 98% on room air. Laboratory evaluation shows: plasma glucose 26.4 mmol/L, venous pH 7.14, serum bicarbonate 9 mmol/L, anion gap 22 mmol/L, serum sodium 134 mmol/L, and serum potassium 3.1 mmol/L. Intravenous access is established, and 1000 mL of 0.9% normal saline is running. What is the most appropriate next step in pharmacological management?

Hold insulin administration, continue isotonic saline rehydration, and begin monitored intravenous potassium chloride at 10 mmol/h until serum potassium is above 3.5 mmol/L. In diabetic ketoacidosis, total-body potassium stores are profoundly depleted due to ongoing osmotic diuresis and urinary excretion. However, extracellular potassium may initially test in the normal, elevated, or low range due to transcellular shifts driven by acidemia and insulin deficiency. Administering exogenous insulin promotes rapid intracellular potassium uptake via activation of Na+/K+-ATPase. If the baseline serum potassium is below 3.5 mmol/L, starting insulin precipitates severe, sudden hypokalemia, predisposing the patient to lethal cardiac dysrhythmias (such as ventricular tachycardia or ventricular fibrillation) and diaphragmatic respiratory arrest. Therefore, standard international resuscitation guidelines dictate that insulin must be strictly held, fluid resuscitation continued, and monitored intravenous potassium chloride begun at 10 mmol/h, with subsequent replacement adjusted to repeat potassium, renal function and urine output until the serum potassium rises above 3.5 mmol/L. Once potassium exceeds 3.5 mmol/L, insulin infusion may be started at 0.1 units/kg/h while continuing potassium replacement to maintain levels between 4.0 and 5.0 mmol/L. Sodium bicarbonate is not indicated at this venous pH of 7.14, and starting dextrose is inappropriate while plasma glucose remains markedly elevated at 26.4 mmol/L.

Q: A 74-year-old woman with a history of hypertension and Type 2 diabetes is brought from a residential care facility with progressive confusion, lethargy, and decreased oral intake over the past 10 days. On examination, she is stuporous and responsive only to painful stimuli. Vital signs: BP 86/54 mmHg, HR 118 bpm, RR 18 breaths/min, temperature 37.1°C. Laboratory results demonstrate: plasma glucose 46.2 mmol/L, serum sodium 152 mmol/L, serum chloride 114 mmol/L, serum bicarbonate 22 mmol/L, venous pH 7.36, serum creatinine 210 umol/L, and urine ketones negative. What is the primary pathophysiological mechanism and the initial therapeutic strategy distinguishing her condition from diabetic ketoacidosis?

Relative insulin deficiency sufficient to suppress lipolysis and ketogenesis, massive osmotic diuresis producing an 8 to 10 liter fluid deficit, with therapy prioritizing fluid resuscitation and delaying or starting insulin at 0.05 units/kg/h once rehydration is underway. This patient presents with classic Hyperosmolar Hyperglycaemic State (HHS), characterized by extreme hyperglycemia (46.2 mmol/L), marked effective hyperosmolality (> 350 mOsm/kg), absence of significant ketoacidosis (venous pH 7.36, serum bicarbonate 22 mmol/L, negative urine ketones), and altered mental status. The core pathophysiological divergence between HHS and DKA is that in HHS, residual endogenous pancreatic beta-cell insulin secretion remains high enough to suppress hormone-sensitive lipase in adipocytes, thereby halting unchecked lipolysis and hepatic ketogenesis. However, insulin levels are insufficient to mediate peripheral glucose uptake or suppress hepatic gluconeogenesis. Over several days to weeks, extreme glucosuria causes massive osmotic water diuresis, producing extreme intracellular and extracellular dehydration with average fluid deficits of 8 to 10 liters (100 to 200 mL/kg), substantially exceeding the 4 to 6 liter deficit typical of DKA. In managing isolated HHS according to the 2024 consensus guidelines, fluid resuscitation is the cornerstone and must precede or accompany any insulin therapy. Fluid expansion alone often steadily lowers blood glucose by restoring renal perfusion. When insulin is indicated (once the patient is adequately volume-resuscitated and glucose is no longer declining with fluids alone), it is initiated at a lower infusion rate of 0.05 units/kg/h (rather than 0.1 units/kg/h) to avoid precipitous osmolar drops, hypokalemia, and cardiovascular collapse.

Q: A 58-year-old Afro-Caribbean man with long-standing Type 2 diabetes, ischemic cardiomyopathy (left ventricular ejection fraction 32%), and chronic kidney disease stage 3b (eGFR 38 mL/min/1.73 m2, baseline serum creatinine 165 umol/L) is reviewed in the clinic. His HbA1c is 8.6% (70 mmol/mol) on gliclazide 80 mg daily. The clinician decides to optimize his medical regimen to provide cardiorenal protection. Which of the following therapeutic choices and clinical counseling points is most accurate?

Initiate an SGLT2 inhibitor (such as empagliflozin or dapagliflozin) for cardiorenal protection, but counsel the patient regarding the risk of euglycemic DKA and the need to withhold the drug during acute illness or prior to elective surgery. SGLT2 inhibitors (such as empagliflozin and dapagliflozin) have revolutionized the management of Type 2 diabetes complicated by heart failure with reduced ejection fraction (HFrEF) and chronic kidney disease. Large landmark clinical trials demonstrated that SGLT2 inhibitors significantly reduce heart failure hospitalizations, slow the decline of renal function, and decrease cardiovascular mortality, with benefits extending to patients with eGFR down to 20-25 mL/min. However, clinicians must educate patients on the risk of euglycemic diabetic ketoacidosis (euDKA), where ketosis occurs with normal or only mildly elevated blood glucose levels. SGLT2 inhibitors must be withheld at least 3 to 4 days prior to elective surgery or during periods of acute dehydration and critical illness. High-dose metformin (2000 mg) is contraindicated at an eGFR of 38 mL/min (maximum recommended dose is 1000 mg daily, and avoided if eGFR < 30 mL/min due to lactic acidosis risk). Glibenclamide is contraindicated in renal impairment due to accumulation of active metabolites causing prolonged hypoglycemia, and sulfonylureas do not reduce heart failure hospitalizations.

Key Takeaways

Diabetes mellitus is diagnosed by fasting plasma glucose >= 7.0 mmol/L, 2-hour post-OGTT glucose >= 11.1 mmol/L, HbA1c >= 6.5% (48 mmol/mol), or random plasma glucose >= 11.1 mmol/L with classic osmotic symptoms.
DKA combines severe insulin deficiency, ketosis and metabolic acidosis; mild DKA can have bicarbonate 15–18 mmol/L. HHS features glucose >= 33.3 mmol/L, effective osmolality > 300 or total > 320 mOsm/kg, beta-hydroxybutyrate < 3 mmol/L, pH >= 7.3 and bicarbonate >= 15 mmol/L.
Start isotonic saline or balanced crystalloid with frequent reassessment (usually 500–1000 mL/h initially; smaller boluses in older, cardiac or renal patients); regular insulin must be strictly withheld if baseline serum potassium is below 3.5 mmol/L and monitored IV potassium replacement begun at 10 mmol/h until potassium exceeds 3.5 mmol/L to prevent lethal ventricular arrhythmias and respiratory arrest.
Start IV regular insulin at 0.1 units/kg/h for DKA or mixed DKA/HHS once potassium permits; below glucose 13.9 mmol/L, add dextrose and reduce to 0.05 units/kg/h while clearing ketoacidosis. Isolated HHS uses 0.05 units/kg/h when indicated after initial fluid assessment.
DKA resolves when blood beta-hydroxybutyrate is < 0.6 mmol/L AND (venous pH >= 7.30 OR bicarbonate >= 18 mmol/L). Glucose should ideally also be < 11.1 mmol/L. Do not use the anion gap or urine ketones to define resolution; overlap subcutaneous basal insulin with IV insulin by 1–2 hours.

Last updated: November 2026

Epidemiology & Diagnostic Classification of Diabetes Mellitus

Diabetes is a major public health challenge across Caribbean territories, with prevalence varying by population, age range and survey year. Obesity, dietary change and genetic susceptibility contribute to its burden. Regional clinicians need both ambulatory glycemic management and rapid recognition and treatment of hyperglycemic emergencies.

Diagnostic Criteria for Diabetes Mellitus

According to World Health Organization (WHO) and American Diabetes Association (ADA) standards, diabetes mellitus is diagnosed when any of the following criteria are met:

Fasting Plasma Glucose (FPG): >= 7.0 mmol/L (126 mg/dL) after an overnight fast of at least 8 hours.
2-Hour 75g Oral Glucose Tolerance Test (OGTT): >= 11.1 mmol/L (200 mg/dL).
Glycated Hemoglobin (HbA1c): >= 6.5% (48 mmol/mol), measured by an NGSP-certified assay standardized to the DCCT reference.
Random Plasma Glucose: >= 11.1 mmol/L (200 mg/dL) in a patient presenting with classic symptoms of hyperglycemia (polyuria, polydipsia, nocturia, and unexplained weight loss) or hyperglycemic crisis.

Clinical Rule: In the absence of unequivocal symptomatic hyperglycemia, diagnosis requires two abnormal test results from either the same blood sample or two separate test occasions.

Pathophysiological Distinction: Type 1 vs. Type 2 Diabetes

Type 1 Diabetes Mellitus (T1DM): Characterized by autoimmune destruction of pancreatic beta-cells within the islets of Langerhans, mediated by autoreactive CD4+ and CD8+ T-lymphocytes. Circulating autoantibodies include anti-glutamic acid decarboxylase (anti-GAD65), anti-islet antigen-2 (anti-IA2), anti-zinc transporter 8 (anti-ZnT8), and islet cell antibodies (ICA). Patients have absolute insulin deficiency, low or undetectable C-peptide levels, and an acute propensity for ketoacidosis.
Type 2 Diabetes Mellitus (T2DM): Results from progressive impairment of insulin secretion against a background of chronic peripheral insulin resistance in skeletal muscle, liver, and adipose tissue. Hepatic gluconeogenesis is unsuppressed, and peripheral GLUT4 translocation is diminished. Endogenous insulin commonly remains sufficient to limit ketogenesis but cannot maintain euglycemia; severe illness or marked insulin deficiency can still produce DKA in type 2 diabetes.

Pathophysiological Divergence: DKA vs. HHS

Acute hyperglycemic emergencies represent divergent points on the spectrum of insulin insufficiency, counter-regulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone), and dehydration.

Diabetic Ketoacidosis (DKA)

Severe Insulin Deficiency: Absolute or relative insulin deficiency, together with excess counter-regulatory hormones, permits uncontrolled ketone production. DKA can occur in type 1 or type 2 diabetes.
Lipolysis & Ketogenesis: Unopposed hormone-sensitive lipase in adipose tissue hydrolyzes triglycerides into glycerol and free fatty acids (FFAs). FFAs enter hepatic mitochondria where carnitine palmitoyltransferase-1 (CPT-1) is disinhibited. Unchecked beta-oxidation generates acetyl-CoA in excess of citric acid cycle capacity, shunting substrates into acetoacetate and beta-hydroxybutyrate.
Metabolic Acidosis: Dissociation of ketoacids generates hydrogen ions, consuming bicarbonate and producing a high anion gap metabolic acidosis (Anion Gap = [Na+] - ([Cl-] + [HCO3-]), normal 8-12 mmol/L; in DKA > 10-12 mmol/L). Accumulation of beta-hydroxybutyrate exceeds acetoacetate by up to 10:1 during peak acidosis.
Severity Classification of DKA:
- Mild: Usually alert; pH > 7.25 to < 7.30 or bicarbonate 15–18 mmol/L, with beta-hydroxybutyrate 3–6 mmol/L.
- Moderate: Alert or drowsy; pH 7.00–7.25 or bicarbonate 10 to < 15 mmol/L, with beta-hydroxybutyrate 3–6 mmol/L.
- Severe: pH < 7.00, bicarbonate < 10 mmol/L or beta-hydroxybutyrate > 6 mmol/L; stupor/coma may occur. Not all severity markers must be present; assess the whole clinical state.
Clinical Features: Rapid onset (< 24 to 48 hours), tachypneic Kussmaul respiration (respiratory compensation blowing off volatile CO2), acetone (fruity) breath odor, nausea, vomiting, and prominent abdominal pain secondary to delayed gastric emptying and mesenteric hypoperfusion.

Hyperosmolar Hyperglycaemic State (HHS)

Relative Insulin Deficiency: Residual endogenous pancreatic insulin secretion remains sufficient to suppress adipose lipolysis and hepatic ketogenesis, preventing severe metabolic acidosis. However, insulin levels are insufficient to stimulate peripheral glucose utilization or downregulate hepatic glycogenolysis and gluconeogenesis.
Massive Osmotic Diuresis: Sustained hyperglycemia produces persistent glucosuria exceeding the renal tubular absorptive threshold (typically > 10.0 mmol/L). Glucosuria causes profound osmotic diuresis, with renal water excretion markedly exceeding electrolyte loss.
Extreme Hyperosmolality & Dehydration: The process evolves insidiously over days to weeks. Total body water deficits average 8 to 10 liters (100 to 200 mL/kg), resulting in severe intracellular and extracellular dehydration, plasma hypertonicity, effective serum osmolality > 300 mOsm/kg, or total osmolality > 320 mOsm/kg [Effective = 2 x Na+ + glucose; total adds urea, all in mmol/L], and prerenal azotemia.
Clinical Features: Depressed consciousness, lethargy, focal neurological signs (hemiparesis, hemisensory loss, focal motor seizures mimicking ischemic stroke), chorea, and hypercoagulability predisposing to arterial and venous thromboembolism.

Comprehensive Diagnostic Comparison: DKA Severity & HHS

Diagnostic Parameter	Mild DKA	Moderate DKA	Severe DKA	Hyperosmolar Hyperglycaemic State (HHS)
Diabetes/Glucose	Diabetes history or glucose >= 11.1 mmol/L (200 mg/dL)	Same DKA criterion	Same DKA criterion	Glucose >= 33.3 mmol/L (600 mg/dL)
Venous pH	> 7.25 to < 7.30	7.00 to 7.25	< 7.00	>= 7.30
Serum Bicarbonate	15–18 mmol/L	10 to < 15 mmol/L	< 10 mmol/L	>= 15 mmol/L
Blood Beta-HB	3.0–6.0 mmol/L	3.0–6.0 mmol/L	> 6.0 mmol/L	< 3.0 mmol/L
Urine Ketones	Usually >= 2+	Usually >= 2+	Usually >= 2+	< 2+ if used instead of blood ketones
Osmolality	Variable	Variable	Variable	Effective > 300 OR total > 320 mOsm/kg
Anion Gap	Usually elevated; not required when ketones measured	Same	Same	Variable
Mental Status	Usually alert	Alert or drowsy	Stupor or coma	Cognitive change common, not required for diagnosis
Typical Fluid Deficit	About 4–6 L	About 4–6 L	About 4–6 L	About 8–10 L; individualize replacement

DKA requires diabetes/hyperglycemia plus ketosis plus acidosis (pH < 7.30 or bicarbonate < 18); do not require every severity marker simultaneously. HHS requires all four diagnostic components. Assess mixed DKA/HHS when significant ketosis or acidosis accompanies hyperosmolality.

Acute Emergency Resuscitation Protocol

Successful management requires systematic, simultaneous restoration of intravascular volume, correction of electrolyte disturbances, suppression of ketogenesis, and prevention of iatrogenic complications, strictly aligned with the 2024 ADA/EASD/JBDS/AACE/DTS multi-society consensus.

1. Intravenous Crystalloid Resuscitation

Initial Replacement: In adults without cardiac or renal compromise, begin isotonic saline or balanced crystalloid at 500–1000 mL/h for the first 2–4 hours. Reassess BP, pulse, perfusion and urine output frequently. Older adults and patients with heart failure or advanced kidney disease need smaller reassessed boluses, for example 250 mL, to avoid overload.
Subsequent Fluids: Adjust to hydration, input/output, sodium and osmolality trends; replace the deficit over about 24–48 hours. A rise in sodium as glucose falls is expected and does not alone justify half-normal saline. In HHS, use 0.45% NaCl only if osmolality fails to decline despite adequate positive fluid balance and appropriate insulin.
HHS Safety: Fluids are the priority and may lower glucose without insulin (often about 2.8–3.9 mmol/L/h, sometimes faster in HHS). Avoid glucose declines > 5–6.7 mmol/L/h, sodium declines > 10 mmol/L in 24 hours, or osmolality declines > 8 mOsm/kg/h. Target an osmolality fall of 3–8 mOsm/kg/h, following serial clinical and biochemical response.
Dextrose Transition: In DKA, when glucose is < 13.9 mmol/L (250 mg/dL), add 5–10% dextrose to replacement fluid and reduce insulin to 0.05 units/kg/h. Continue enough insulin to clear ketoacidosis while maintaining glucose near 11.1 mmol/L. In HHS, add dextrose as glucose approaches the treatment target so ongoing correction of hyperosmolality does not cause hypoglycemia.

2. Potassium Protocol (The Critical Pre-Insulin Requirement)

Total-body potassium is depleted by osmotic diuresis, even when serum potassium is initially normal or high. Insulin and correction of acidosis move potassium into cells, so replacement and monitoring must accompany treatment.

K < 3.5 mmol/L: HOLD INSULIN, including boluses. Continue fluid resuscitation and begin monitored IV potassium at 10 mmol/h; delay insulin until K > 3.5 mmol/L. Adjust replacement to repeat potassium, renal function, urine output and the monitored local protocol.
K 3.5 to < 5.0 mmol/L: Usually add 20–30 mmol potassium per litre of replacement fluid to maintain K 4–5 mmol/L.
K >= 5.0 mmol/L: Initially withhold potassium; start replacement when it falls below 5.0 mmol/L. Check potassium 2 hours after starting insulin and at least every 4 hours during treatment, more frequently for low potassium or rapid change. Concentration (mmol/L) and delivery rate (mmol/h) are distinct and must be calculated from the fluid rate.

3. Insulin Dosing: DKA vs. Isolated HHS

For DKA and Mixed DKA/HHS:
- Once potassium permits, start IV regular insulin at 0.1 units/kg/h. The aim is to suppress ketogenesis and correct acidosis. In HHS, beta-hydroxybutyrate >= 3 mmol/L, urine ketones >= 2+, pH < 7.3 or bicarbonate < 18 selects this mixed-crisis insulin pathway.
- Check glucose every 1–2 hours and follow electrolytes, venous pH and blood ketones. If response is inadequate, reassess fluids, IV delivery and the precipitant, then adjust insulin using the monitored protocol.
- When glucose falls below 13.9 mmol/L (250 mg/dL), add 5–10% dextrose and reduce insulin to 0.05 units/kg/h, adjusting to maintain glucose near 11.1 mmol/L until ketoacidosis resolves.
For Isolated HHS:
- Fluid resuscitation is the cornerstone. Insulin should NOT be started immediately if fluid resuscitation alone is effectively lowering blood glucose. In isolated HHS, early aggressive insulin administration before volume repletion risks circulatory collapse (as glucose and water shift into cells, depleting intravascular volume) and rapid osmolar shifts.
- When insulin is initiated (after initial fluid expansion and once glucose is no longer falling adequately with fluids alone, or concurrently after volume repletion), the starting dose for isolated HHS is 0.05 units/kg/hour (NOT 0.1 units/kg/hour).
- Target a gradual plasma glucose decline of 3.0 to 5.0 mmol/L/hour, avoiding precipitous drops that heighten the risk of neurological complications.

4. Sodium Bicarbonate: Narrow Indications

Routine bicarbonate is not recommended: fluids and insulin usually correct DKA acidosis, and bicarbonate can worsen hypokalemia, impair oxygen delivery and cause paradoxical CNS acidosis.
Consider bicarbonate for severe acidosis (pH < 7.0) with close monitoring. If indicated, give 100 mmol sodium bicarbonate in 400 mL sterile water, reassessing and repeating every 2 hours until pH > 7.0. Manage potassium according to measured levels rather than adding a fixed dose regardless of serum K.

5. Resolution Criteria & Transition to Subcutaneous Insulin

DKA Resolution: Require blood beta-hydroxybutyrate < 0.6 mmol/L AND (venous pH >= 7.30 OR bicarbonate >= 18 mmol/L). Glucose should ideally also be < 11.1 mmol/L (200 mg/dL). Ketone clearance is required, not an optional third test. Do not use the anion gap or urine ketones to define resolution: saline can cause hyperchloremic acidosis, while beta-hydroxybutyrate converts to urine-detectable acetoacetate during recovery.
HHS Resolution: The consensus proposes measured/calculated osmolality < 300 mOsm/kg, glucose < 13.9 mmol/L (250 mg/dL), urine output > 0.5 mL/kg/h and improved cognition. Assess volume and clinical recovery alongside these measures.
Subcutaneous Overlap: Administer a subcutaneous dose of intermediate- or long-acting basal insulin (or resume home basal-bolus regimen) 1 to 2 hours BEFORE discontinuing the IV insulin infusion. Immediate cessation of IV insulin without overlap leads to rapid rebound ketoacidosis due to the extremely short circulating half-life of intravenous regular insulin (under 5-9 minutes).

Long-Term Pharmacotherapy for Type 2 Diabetes

Modern pharmacological management of T2DM balances glycemic reduction with cardiorenal organ protection.

Metformin (Biguanide): First-line agent worldwide. Activates AMP-activated protein kinase (AMPK), reducing hepatic gluconeogenesis and improving peripheral insulin sensitivity. Weight-neutral with minimal hypoglycemia risk.
- Renal Restrictions: Check baseline eGFR. Dose reduction recommended if eGFR is 30 to 44 mL/min (maximum 1000 mg daily); contraindicated if eGFR < 30 mL/min due to risk of metformin-associated lactic acidosis (MALA). Temporarily withhold before iodinated radiocontrast procedures in patients with eGFR < 60 mL/min.
SGLT2 Inhibitors (Empagliflozin, Dapagliflozin, Canagliflozin): Inhibit sodium-glucose cotransporter 2 in the renal proximal convoluted tubule, inducing glucosuria and natriuresis. Provide profound cardiorenal benefits: reduce heart failure hospitalizations, slow progression of chronic kidney disease, and decrease cardiovascular mortality.
- Adverse Effects & Risks: Mycotic genital infections (candidiasis), urinary tract infections, volume depletion, and euglycemic DKA (euDKA). In euDKA, profound ketosis occurs with plasma glucose < 11.1 mmol/L (200 mg/dL) due to persistent renal glucose clearance. SGLT2 inhibitors must be withheld at least 3 to 4 days prior to elective surgery or during acute severe medical illness.
GLP-1 Receptor Agonists (Liraglutide, Semaglutide, Dulaglutide): Incretin mimetics that bind the GLP-1 receptor, augmenting glucose-dependent insulin secretion, suppressing postprandial glucagon, and slowing gastric emptying. Promote substantial weight loss and provide proven major adverse cardiovascular event (MACE) reduction in patients with established atherosclerotic cardiovascular disease.
- Adverse Effects: Gastrointestinal symptoms (nausea, vomiting), risk of pancreatitis; contraindicated in individuals with personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia type 2 (MEN 2).
Sulfonylureas (Gliclazide, Glimepiride, Glibenclamide): Bind the SUR1 subunit of beta-cell ATP-sensitive K+ channels to stimulate insulin secretion. Associated with hypoglycemia and weight gain. Gliclazide is preferred over glibenclamide in elderly patients or mild renal dysfunction due to shorter half-life and lower risk of prolonged hypoglycemia.
DPP-4 Inhibitors (Sitagliptin, Linagliptin): Inhibit dipeptidyl peptidase-4, prolonging endogenous GLP-1 activity. Weight-neutral with low hypoglycemia risk. Linagliptin is eliminated via the enterohepatic system and requires no dose adjustment across all stages of renal disease.

Loading diagram...

Emergency Hyperglycemic Crisis Resuscitation Pathway (DKA & HHS)

Test Your Knowledge

A 19-year-old man with Type 1 diabetes is brought to the emergency department after 2 days of vomiting, polyuria, and progressive breathlessness. On physical examination, he appears severely dehydrated with dry mucous membranes and deep, rapid breathing. Vital signs: BP 96/60 mmHg, HR 122 bpm, RR 30 breaths/min, SpO2 98% on room air. Laboratory evaluation shows: plasma glucose 26.4 mmol/L, venous pH 7.14, serum bicarbonate 9 mmol/L, anion gap 22 mmol/L, serum sodium 134 mmol/L, and serum potassium 3.1 mmol/L. Intravenous access is established, and 1000 mL of 0.9% normal saline is running. What is the most appropriate next step in pharmacological management?

Administer an intravenous bolus of regular insulin at 0.1 units/kg followed immediately by a continuous infusion at 0.1 units/kg/h

Hold insulin administration, continue isotonic saline rehydration, and begin monitored intravenous potassium chloride at 10 mmol/h until serum potassium is above 3.5 mmol/L

Administer 100 mmol of sodium bicarbonate diluted in sterile water over 2 hours to correct severe acidemia

Start an intravenous infusion of 5% dextrose in water at 100 mL/h and begin subcutaneous insulin glargine

Test Your Knowledge

A 74-year-old woman with a history of hypertension and Type 2 diabetes is brought from a residential care facility with progressive confusion, lethargy, and decreased oral intake over the past 10 days. On examination, she is stuporous and responsive only to painful stimuli. Vital signs: BP 86/54 mmHg, HR 118 bpm, RR 18 breaths/min, temperature 37.1°C. Laboratory results demonstrate: plasma glucose 46.2 mmol/L, serum sodium 152 mmol/L, serum chloride 114 mmol/L, serum bicarbonate 22 mmol/L, venous pH 7.36, serum creatinine 210 umol/L, and urine ketones negative. What is the primary pathophysiological mechanism and the initial therapeutic strategy distinguishing her condition from diabetic ketoacidosis?

Absolute insulin deficiency causing severe peripheral lipolysis, with priority given to immediate high-dose insulin bolus prior to intravenous fluid resuscitation

Profound unsuppressed hepatic ketogenesis causing high anion gap acidosis, with a fluid deficit of 4 to 6 liters requiring early sodium bicarbonate infusion

Excessive counter-regulatory growth hormone secretion causing central diabetes insipidus, requiring immediate desmopressin and rapid hypotonic fluid administration

Relative insulin deficiency sufficient to suppress lipolysis and ketogenesis, massive osmotic diuresis producing an 8 to 10 liter fluid deficit, with therapy prioritizing fluid resuscitation and delaying or starting insulin at 0.05 units/kg/h once rehydration is underway

Test Your Knowledge

A 58-year-old Afro-Caribbean man with long-standing Type 2 diabetes, ischemic cardiomyopathy (left ventricular ejection fraction 32%), and chronic kidney disease stage 3b (eGFR 38 mL/min/1.73 m2, baseline serum creatinine 165 umol/L) is reviewed in the clinic. His HbA1c is 8.6% (70 mmol/mol) on gliclazide 80 mg daily. The clinician decides to optimize his medical regimen to provide cardiorenal protection. Which of the following therapeutic choices and clinical counseling points is most accurate?

Initiate an SGLT2 inhibitor (such as empagliflozin or dapagliflozin) for cardiorenal protection, but counsel the patient regarding the risk of euglycemic DKA and the need to withhold the drug during acute illness or prior to elective surgery

Initiate high-dose metformin at 2000 mg daily, as it is the safest first-line agent across all stages of renal disease and provides superior heart failure mortality reduction

Start linagliptin combined with glibenclamide, as sulfonylureas provide proven reduction in heart failure hospitalizations in patients with reduced ejection fraction

Initiate exenatide twice daily, advising the patient that GLP-1 receptor agonists are strictly contraindicated if eGFR is above 30 mL/min

Sections you finish are checked off in the contents.

Up Next

4.2 Thyroid Disorders: Thyrotoxicosis, Hypothyroidism & Thyroid Storm

Continue learning