When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EMERGENTEndocrine

Inpatient Hypoglycemia

The most common inpatient endocrine emergency. Every episode of glucose < 70 requires intervention. Recurrent hypoglycemia increases mortality independent of the cause.

🔍 Overview

Overview

Inpatient hypoglycemia (glucose < 70 mg/dL) affects up to 10-30% of hospitalized diabetic patients and is independently associated with increased mortality, longer LOS, and ICU transfer. NICE-SUGAR, NEJM 2009 Classified as: Level 1 (54-70 mg/dL, alert), Level 2 (< 54, clinically significant), Level 3 (severe, requiring assistance from another person). Most common causes: (1) insulin-food mismatch (holding meals while continuing insulin), (2) renal insufficiency (reduced insulin clearance), (3) reduced PO intake (NPO, nausea, surgery), (4) medication errors. Key principle: every hypoglycemic event is preventable and deserves root cause analysis. The attending will ask "why did this happen and what did you change?"

🧪 Workup

Workup

Confirm with venous glucose -point-of-care glucometers are less accurate at low ranges. Whipple's triad: symptoms + low glucose + symptom resolution with glucose correction.
Review insulin/secretagogue doses -#1 cause. Check timing of last insulin dose vs last meal. Basal insulin too high? Sliding scale overlapping with scheduled dose?
BMP -Cr (AKI/CKD reduces insulin clearance → prolonged insulin effect), hepatic function (reduced gluconeogenesis)
Medication reconciliation -sulfonylureas (long-acting, especially in CKD), insulin dose errors, fluoroquinolones (rare), pentamidine, beta-blockers (mask symptoms)
NPO status -was patient made NPO for procedure while basal insulin continued?
Nutrition assessment -decreased PO intake, skipped meals, vomiting, new tube feed interruption
If non-diabetic unexplained hypoglycemia: insulin level + C-peptide + proinsulin + sulfonylurea screen (draw DURING hypoglycemia). High insulin + high C-peptide = endogenous hyperinsulinism (insulinoma). High insulin + low C-peptide = exogenous insulin. High C-peptide + positive SU screen = sulfonylurea use.
Cortisol -if adrenal insufficiency suspected (especially if recurrent hypoglycemia with hypotension)

🚨 Management

Management

Unable to eat / AMS / NPO: D50W 25g (50 mL) IV push → recheck in 15 min → repeat PRN → start D10W drip at 50-100 mL/hr if recurrent

No IV access: Glucagon 1 mg IM/SQ. Causes nausea -position on side.

Prevent recurrence (most important step):

Reduce basal insulin by 20-40% if the episode occurred overnight or fasting ADA Standards of Care, 2026
Hold or reduce prandial insulin if patient is eating less than usual or NPO
Discontinue sulfonylurea in CKD/AKI (long half-life → recurrent hypoglycemia for 24-72h)
Adjust sliding scale -reduce correction factor if consistently hypoglycemic
Ensure meal delivery before prandial insulin -coordinate with nursing
Hold prandial insulin if patient is NPO -only continue basal (and reduce by 20-50%)

Document root cause analysis in the note -attendings expect it.

Sulfonylurea-induced hypoglycemia (especially glipizide/glyburide in CKD) can recur for 24-72 hours even after initial correction. These patients need D10 drip + hourly glucose checks + admission for observation. Octreotide 50 mcg SQ q6h can reduce insulin secretion in refractory cases.

Monitoring

💊 Medications

Medications

Drug	Dose	Route	Notes
D50W (Dextrose 50%)	25g (50 mL) IV push	IV	First-line for severe/unable to eat. Repeat q15min PRN. Causes phlebitis -use large bore IV.
D10W drip	50-100 mL/hr	IV	For recurrent hypoglycemia (especially sulfonylurea-induced). Prevents repeated D50 pushes.
Glucagon	1 mg IM/SQ	IM/SQ	If no IV access. Mobilizes hepatic glycogen. Ineffective if glycogen-depleted (alcoholics, liver failure). Causes nausea.
Octreotide (Sandostatin)	50 mcg SQ q6h	SQ	For sulfonylurea-induced hypoglycemia refractory to D10. Suppresses insulin release from pancreatic beta cells. McLaughlin, 2000
Oral glucose (juice/tabs)	15-20g fast-acting carbs	PO	First-line if alert + able to swallow. Follow with complex carbs. Recheck at 15 min.

🏥 Rounds

Pimp Questions

❓ Why is sulfonylurea-induced hypoglycemia more dangerous than insulin-induced?

Sulfonylureas (especially glyburide and glipizide) have long half-lives (12-24h+) that are prolonged further in CKD. Unlike insulin which has a predictable duration, sulfonylureas can cause recurrent hypoglycemia for 24-72 hours even after initial correction. This is why patients need D10 drip + observation, not just a D50 push and discharge. Octreotide can help by suppressing insulin release.

❓ How do you differentiate insulinoma from exogenous insulin administration?

Draw labs during hypoglycemia: Insulinoma: high insulin + high C-peptide + high proinsulin (endogenous production). Exogenous insulin: high insulin + LOW C-peptide (exogenous insulin suppresses endogenous production). Sulfonylurea use: high insulin + high C-peptide + positive sulfonylurea screen. C-peptide is the key differentiator because commercial insulin preparations do not contain C-peptide.

❓ When should you use octreotide for hypoglycemia?

Sulfonylurea-induced hypoglycemia refractory to D10 drip. Octreotide (somatostatin analog) suppresses insulin secretion from pancreatic beta cells. Dose: 50 mcg SQ q6h. It is NOT useful for insulin-induced hypoglycemia (the problem is exogenous insulin, not endogenous secretion). Consider in: recurrent hypoglycemia despite D10, glipizide/glyburide with CKD, intentional sulfonylurea ingestion. McLaughlin, 2000

❓ What insulin adjustments should you make after an inpatient hypoglycemic event?

Root cause analysis + immediate order changes: (1) If overnight/fasting hypo → reduce basal insulin by 20-40%. (2) If post-prandial hypo → reduce prandial/correction dose. (3) If NPO → hold prandial, reduce basal by 20-50%. (4) If on sulfonylurea + AKI/CKD → STOP sulfonylurea. (5) If multiple sliding scale corrections overlapping → simplify regimen. Document the analysis and changes in your note -this is expected by attendings.

❓ Why does glucagon not work in alcoholic or liver failure patients?

Glucagon works by mobilizing hepatic glycogen stores (glycogenolysis). In chronic alcoholics and liver failure patients, glycogen stores are depleted (alcohol inhibits gluconeogenesis + poor nutritional intake). Without glycogen to break down, glucagon is ineffective. These patients need IV dextrose (D50 or D10 drip) -there is no alternative.

❓ What is the "rule of 15" for hypoglycemia?

For alert patients who can eat: give 15 grams of fast-acting carbohydrate (4 oz juice, 3-4 glucose tabs) → recheck glucose in 15 minutes → repeat if still < 70. Once glucose > 70, follow with a complex carbohydrate snack to prevent recurrence. Simple and effective -but only works if the patient can protect their airway and swallow safely.

Sample Presentation

Mr. Garcia is a 68-year-old man with T2DM on glargine 40 units + glipizide 10 mg BID, admitted for pneumonia, found to have fingerstick glucose of 38 at 3 AM. Diaphoretic, confused. Last meal was dinner at 5 PM (ate 50% of tray). Cr 2.4 (baseline 1.2). Received full sliding scale correction of 6 units at 9 PM for glucose of 220.

Key Points: Three contributors: (1) Glipizide in AKI (reduced clearance → prolonged hypoglycemic effect), (2) reduced PO intake, (3) sliding scale correction on top of basal + sulfonylurea. Immediate: D50 25g IV → start D10 drip. Prevent: STOP glipizide (always in AKI). Reduce glargine by 40% (24 units). Reduce sliding scale. This patient needs q1h glucose checks × 24h because glipizide will continue to cause hypoglycemia.

Fingerstick glucose q15 min until glucose > 100 and stable
Then q1h × 4h to ensure no recurrence (especially with long-acting insulin or sulfonylureas)
Resume regular glucose monitoring (AC/HS or q6h) once stable
Review all insulin orders after ANY hypoglycemic event -this is the intern's most important action
Notify attending of any Level 2 (< 54) or Level 3 (severe) hypoglycemia
Hypoglycemia event report -many hospitals require formal incident reporting
Pre-prandial glucose + post-meal check if adjusting regimen -verify effectiveness of changes
A1c -helps guide discharge insulin regimen (A1c < 7% on insulin = possibly over-basal'd)

Monitoring

📋 Summary

Summary

Definition

Glucose < 70. Level 1: 54-70. Level 2: < 54. Level 3: needs help.

Treat

Alert: 15g carbs PO. Unable to eat: D50 25g IV. No IV: glucagon 1 mg IM. Recurrent: D10 drip.

Prevent

Reduce basal 20-40%. Stop SU in CKD. Hold prandial if NPO. Review all insulin orders.

SU Danger

Recurs × 24-72h (long half-life + CKD). D10 drip + octreotide 50 mcg q6h.

Root Cause

Document: insulin-food mismatch, NPO status, AKI, med error, reduced PO intake.

Pearl

Every hypo event is preventable. The attending will ask what you changed.

📄 One Pager

One-Pager

Inpatient Hypoglycemia

Treat, prevent, document

Immediate

Alert: 15g PO carbs → recheck 15 min. AMS/NPO: D50 25g IV → repeat PRN → D10 drip. No IV: glucagon 1 mg IM.

Prevent Recurrence

Reduce basal 20-40%. STOP sulfonylurea in AKI. Hold prandial if NPO. Ensure meal before prandial insulin. SU hypo: D10 drip + octreotide + observe 24-72h.

Workup If Non-Diabetic

Draw DURING hypo: insulin, C-peptide, proinsulin, sulfonylurea screen. High insulin + low C-peptide = exogenous. High insulin + high C-peptide = insulinoma or SU.