The "Sick Day Rule" in Diabetes Management: A Practical Framework for Preventing Acute Hyperglycemic Crises

Dr Neeraj Manikath , calude.ai

Abstract

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) represent preventable yet frequently encountered acute complications of diabetes mellitus, accounting for substantial morbidity, mortality, and healthcare costs. The "sick day rule"—a structured patient education intervention providing clear guidelines for diabetes self-management during intercurrent illness—has emerged as a critical preventive strategy. This review synthesizes the evidence supporting sick day management protocols, provides a practical framework for implementation, and offers clinical pearls for postgraduate physicians to enhance patient education and prevent acute hyperglycemic emergencies.

Introduction

Every year, approximately 200,000 hospital admissions in the United States are attributed to DKA, with HHS accounting for an additional 15,000-20,000 hospitalizations.¹ Despite advances in diabetes care, these acute complications continue to burden healthcare systems, with mortality rates of 1-5% for DKA and 10-20% for HHS.²,³ The tragedy lies not in the complexity of prevention but in the simplicity of what we often fail to communicate: structured sick day management.

The physiological stress response during acute illness—characterized by elevated counter-regulatory hormones (cortisol, glucagon, catecholamines, growth hormone)—creates a perfect storm for metabolic decompensation in diabetes patients.⁴ Infection, trauma, myocardial infarction, or even minor viral illnesses trigger increased hepatic glucose production, enhanced lipolysis, and relative insulin resistance. Without appropriate intervention, this cascade progresses to hyperglycemia, osmotic diuresis, dehydration, and potentially life-threatening metabolic acidosis or hyperosmolarity.⁵

The Evidence Base for Sick Day Rules

Efficacy in Preventing Hospitalizations

A landmark study by Laffel et al. demonstrated that structured sick day management education reduced DKA episodes by 58% in pediatric type 1 diabetes populations over a two-year follow-up period.⁶ Similar benefits have been observed in adult populations, with a Dutch cohort study showing a 43% reduction in DKA admissions following implementation of standardized sick day protocols in primary care.⁷

The mechanism of benefit is straightforward: early recognition of deteriorating metabolic control, aggressive hydration, and appropriate insulin adjustment prevent the progression from hyperglycemia to ketoacidosis or hyperosmolarity. The intervention is cost-effective, with one economic analysis demonstrating savings of approximately $8,400 per DKA admission prevented.⁸

Components of Effective Sick Day Management

The American Diabetes Association (ADA) and the Joint British Diabetes Societies (JBDS) both emphasize structured sick day protocols as standard of care.⁹,¹⁰ Core components consistently identified across guidelines include:

Increased frequency of glucose monitoring
Ketone monitoring when indicated
Aggressive hydration strategies
Continuation (and often intensification) of basal insulin
Recognition of warning signs requiring medical attention
Appropriate medication adjustments

The Sick Day Rule Framework: Component Analysis

Rule 1: Check Blood Sugar Every 2-4 Hours

Rationale: Standard glucose monitoring intervals (fasting, pre-meal, bedtime) are inadequate during physiological stress. Counter-regulatory hormones can cause rapid glucose excursions, and the hyperglycemia may be masked by reduced oral intake.

Pearl: Advise patients to set smartphone alarms every 3 hours, including overnight checks if glucose trends upward. Continuous glucose monitors (CGMs) offer superior real-time data during sick days, with studies showing CGM use reduces DKA risk by 60% compared to fingerstick monitoring alone.¹¹

Oyster: Patients often reduce monitoring when feeling unwell. Reframe this as "Your meter is your medical team when we can't be there." Make it personal.

Rule 2: Check Ketones if Blood Sugar >250 mg/dL

Rationale: Ketogenesis begins when insulin deficiency causes preferential lipid metabolism. Ketone monitoring allows early detection of metabolic decompensation before clinical acidosis develops.

Evidence: Blood beta-hydroxybutyrate (β-OHB) measurement is superior to urine ketone testing, with better correlation to DKA severity.¹² However, urine ketone strips remain acceptable when blood ketone meters are unavailable. A β-OHB level >1.5 mmol/L or moderate/large urine ketones warrant immediate medical contact.

Hack: For type 2 diabetes patients not on insulin, ketone monitoring may seem counterintuitive—but HHS can occur without significant ketosis. Emphasize that glucose >300 mg/dL in type 2 diabetes during illness still warrants medical evaluation, even without ketones.

Clinical Teaching Point: SGLT2 inhibitor use has introduced euglycemic DKA—a dangerous scenario where ketoacidosis develops despite near-normal glucose levels (140-250 mg/dL).¹³ Always check ketones in SGLT2-treated patients during illness, regardless of glucose level.

Rule 3: Drink Sugar-Free Fluids Every Hour

Rationale: Osmotic diuresis from hyperglycemia causes profound volume depletion—often 5-10 liters in DKA and up to 15 liters in HHS.¹⁴ Early aggressive oral hydration prevents progression to severe dehydration requiring intravenous therapy.

Specific Recommendations:

Target: 8-12 ounces (240-360 mL) of fluid hourly while awake
Options: Water, sugar-free electrolyte drinks, clear broth
Avoid: Fruit juice, regular soda, milk (adds glucose/osmotic load)

Pearl: If patients cannot tolerate plain water due to nausea, recommend:

Electrolyte popsicles (sugar-free)
Diluted broth (provides sodium to combat urinary losses)
Small sips of water every 10-15 minutes rather than large volumes

Hack: Give patients a concrete visual: "Fill a 2-liter bottle with water in the morning. Your goal is to empty it by bedtime."

Rule 4: Never Skip Basal/Long-Acting Insulin

Rationale: This is the most counterintuitive yet critical rule. Patients instinctively reduce or omit insulin when eating poorly, not realizing that basal insulin suppresses hepatic glucose production and lipolysis independent of carbohydrate intake.⁴

Evidence: Insulin omission is the leading precipitant of DKA in young adults with type 1 diabetes, accounting for 30-40% of episodes.¹⁵ During illness, insulin requirements typically increase by 20-50% due to stress hormones.⁴

Teaching Approach: Use this metaphor: "Basal insulin is like your home's heating system—it runs constantly to maintain the environment. Mealtime insulin is like turning up the thermostat when you cook. When you're sick, your body's 'thermostat' is broken, and you need more baseline heating, not less."

Practical Adjustment Protocol:

If glucose >250 mg/dL: Increase basal insulin by 10-20%
If moderate/large ketones present: Increase by 20% and give supplemental rapid-acting insulin
Continue basal insulin even if NPO (nothing by mouth)

Oyster: For pump users, sick days require special vigilance. Pump failure (kinked catheter, site infection) can cause DKA within 4-6 hours due to lack of subcutaneous insulin depot.¹⁶ Teach pump users: "If glucose >250 with ketones, inject insulin with a pen/syringe immediately while troubleshooting the pump."

Rule 5: Call Your Doctor If...

Critical Warning Signs:

Inability to retain fluids (persistent vomiting)
Blood glucose >250 mg/dL for >12 hours despite insulin adjustments
Moderate or large ketones (urine) or β-OHB >1.5 mmol/L (blood)
Confusion, altered mental status, or severe lethargy
Abdominal pain, rapid breathing, or fruity breath odor (DKA signs)

Teaching Hack: Use the acronym "FLUIDS" for when to call:

Fluids won't stay down
Levels (glucose) stay high (>250 x 12 hours)
Unusual confusion or drowsiness
Increased ketones
Difficulty breathing
Severe abdominal pain

Pearl: Establish a clear communication plan. Provide direct phone numbers (not general clinic lines) and define expected response times. Consider text-based monitoring systems for high-risk patients during sick days.

Medication Adjustments: The SADMANS Mnemonic

During acute illness with dehydration risk, certain medications require temporary discontinuation. The mnemonic SADMANS guides this:¹⁷

SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin)
ACE inhibitors/ARBs
Diuretics
Metformin
Aldosterone antagonists
NSAIDs
Sodium-glucose transport inhibitors (redundant with S, but emphasizes SGLT2)

For Diabetes Specifically:

SGLT2 Inhibitors: STOP during any illness with volume depletion risk or when NPO. These agents increase glucosuria-induced dehydration and euglycemic DKA risk.¹³,¹⁸ Resume only after patient is eating/drinking normally for 24-48 hours.

Metformin: STOP if vomiting, diarrhea, or significant dehydration due to lactic acidosis risk, particularly with renal hypoperfusion.¹⁹ Lactic acidosis mortality approaches 50%, making this a critical intervention.

Continue These Medications:

All insulin (as discussed)
Sulfonylureas (with glucose monitoring due to hypoglycemia risk if not eating)
DPP-4 inhibitors
GLP-1 receptor agonists (though may worsen nausea)

Hack: Create a wallet card for patients listing their diabetes medications with colored dots: Green = continue, Red = stop when sick, Yellow = continue but watch for low blood sugar.

Implementation Strategy: Making Sick Day Rules Stick

The Educational Encounter

Teach-Back Method: After explaining sick day rules, ask: "Can you explain back to me what you'll do if you wake up with the flu and your sugar is 280?" This validates understanding and identifies knowledge gaps. Studies show teach-back improves diabetes self-management behaviors by 35%.²⁰

Written Handout: Verbal instructions have <20% retention after 48 hours.²¹ Provide a one-page, literacy-appropriate handout (6th-8th grade reading level) in the patient's preferred language.

Timing: Provide sick day education at:

Diabetes diagnosis
Every annual comprehensive diabetes visit
Hospital discharge (especially post-DKA/HHS)
When prescribing SGLT2 inhibitors

Sample One-Page Handout Structure

Header: "My Sick Day Plan for Diabetes" with space for patient name and date

Section 1: When to Use This Plan (fever, vomiting, infection, flu, injury)

Section 2: The 5 Rules (numbered, large font, checkboxes)

Section 3: Medications to STOP (red box): SGLT2 inhibitors, metformin if vomiting

Section 4: Emergency Contact Numbers (physician, diabetes educator, emergency department)

Section 5: Insulin Adjustment Table:

Blood Sugar	Ketones	Action
150-250	None	Continue usual insulin
250-350	Small/None	Increase basal by 10%, check again in 3h
>350 or any	Moderate/Large	Call doctor NOW

Technology Integration

CGM Alerts: Program high glucose alerts at 250 mg/dL during illness. Share CGM data with providers remotely for real-time guidance.

Telemedicine: Sick day management is ideally suited for virtual visits. Video assessment can identify altered mental status, tachypnea, or severe distress, triaging who needs emergency evaluation versus home management.²²

Apps: Several diabetes management apps include sick day modules with automated reminders and decision support. Integration with electronic health records allows providers to monitor high-risk patients proactively.

Special Populations

Type 2 Diabetes

Many clinicians neglect sick day education in type 2 diabetes, assuming lower DKA risk. This is dangerous—HHS carries higher mortality than DKA.³ Type 2 patients on insulin require identical education to type 1 patients.

Pearl: For non-insulin-treated type 2 diabetes, focus on hydration and medication holds (especially SGLT2 inhibitors). Emphasize glucose threshold for medical contact (>300 mg/dL sustained or any reading >400 mg/dL).

Older Adults

Elderly patients experience disproportionate HHS burden due to impaired thirst mechanisms, polypharmacy, and cognitive barriers to self-management.²³ Involve caregivers in education and consider home health nursing for sick day monitoring in high-risk individuals.

Pregnancy

Pregnant women with pregestational or gestational diabetes develop DKA at lower glucose thresholds (>200 mg/dL) due to accelerated starvation physiology.²⁴ Lower intervention thresholds and immediate obstetric consultation are warranted.

Clinical Pearls and Oysters

Pearl 1: Create a "sick day supply kit" with patients containing glucose meter strips, ketone strips/meter, sugar-free electrolyte drinks, and a laminated instruction card. Review contents annually.

Pearl 2: The most common cause of preventable DKA is insulin pump failure during illness. Teach all pump users to keep injectable insulin available and know their total daily dose (TDD) for emergency conversion.

Pearl 3: Not all hyperglycemia during illness requires increased insulin. Sepsis-induced insulin resistance may require 2-3x usual doses. Work with endocrinology when encountering persistent hyperglycemia (>400 mg/dL) despite appropriate sick day management.

Oyster 1: Patients with gastroparesis may develop "starvation ketosis" during viral illness despite adequate insulin—ketones without hyperglycemia. This doesn't require insulin increases but rather carbohydrate-containing fluids (juice, regular soda) in small, frequent amounts.

Oyster 2: Steroid administration (e.g., prednisone for asthma exacerbation) causes profound insulin resistance, with glucose peaks 4-8 hours post-dose. Preemptively increase insulin by 30-50% on steroid days, with most effect on prandial insulin.²⁵

Oyster 3: Athletic diabetics who develop acute illness often experience rebound hyperglycemia when discontinuing exercise. Their baseline insulin doses may be reduced to accommodate activity; illness requires returning to non-exercise insulin regimens plus sick day adjustments.

Measuring Success: Quality Metrics

Programs implementing standardized sick day education should track:

DKA/HHS admission rates (target: <1% of diabetes population annually)
Emergency department visits for hyperglycemia
Patient knowledge assessment scores (teach-back success rate)
Sick day plan documentation in medical records (target: 100% of insulin-treated patients)

Conclusion

The sick day rule represents low-tech, high-impact medicine. As educators, our responsibility extends beyond prescribing insulin regimens to ensuring patients possess the knowledge and confidence to navigate acute illness independently. The tragedy of preventable DKA is not that the solution is complex—it's that we too often assume patients inherently know to continue insulin, check ketones, and hydrate aggressively.

Make sick day education visible: print handouts in bright colors, laminate them, and place them in every diabetic patient's hands at every opportunity. Role-play scenarios during clinic visits. Use teach-back religiously. Create systems—EMR alerts, standardized discharge protocols, diabetes educator referrals—that ensure no insulin-treated patient leaves our care without this life-saving knowledge.

The "sick day rule" is not merely a patient handout—it's a professional commitment to preventive medicine in its purest form. Master it, teach it, and systematize it. Your patients' lives depend on it.

References

Benoit SR, Zhang Y, Geiss LS, Gregg EW, Albright A. Trends in diabetic ketoacidosis hospitalizations and in-hospital mortality - United States, 2000-2014. MMWR Morb Mortal Wkly Rep. 2018;67(12):362-365.
Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335-1343.
Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014;37(11):3124-3131.
Dungan KM, Braithwaite SS, Preiser JC. Stress hyperglycaemia. Lancet. 2009;373(9677):1798-1807.
Gosmanov AR, Gosmanova EO, Dillard-Cannon E. Management of adult diabetic ketoacidosis. Diabetes Metab Syndr Obes. 2014;7:255-264.
Laffel LM, Wentzell K, Loughlin C, Tovar A, Moltz K, Brink S. Sick day management using blood 3-hydroxybutyrate (3-OHB) compared with urine ketone monitoring reduces hospital visits in young people with T1DM: a randomized clinical trial. Diabet Med. 2006;23(3):278-284.
Vanelli M, Chiari G, Ghizzoni L, Costi G, Giacalone T, Chiarelli F. Effectiveness of a prevention program for diabetic ketoacidosis in children. Diabetes Care. 1999;22(1):7-9.
Rewers A, Chase HP, Mackenzie T, et al. Predictors of acute complications in children with type 1 diabetes. JAMA. 2002;287(19):2511-2518.
American Diabetes Association. 6. Glycemic targets: Standards of Medical Care in Diabetes—2024. Diabetes Care. 2024;47(Suppl 1):S111-S125.
Joint British Diabetes Societies Inpatient Care Group. The management of diabetic ketoacidosis in adults. 2021. Available at: https://abcd.care/resource/management-diabetic-ketoacidosis-dka-adults
Bergenstal RM, Klonoff DC, Garg SK, et al. Threshold-based insulin-pump interruption for reduction of hypoglycemia. N Engl J Med. 2013;369(3):224-232.
Sheikh-Ali M, Karon BS, Basu A, et al. Can serum beta-hydroxybutyrate be used to diagnose diabetic ketoacidosis? Diabetes Care. 2008;31(4):643-647.
Peters AL, Buschur EO, Buse JB, Cohan P, Diner JC, Hirsch IB. Euglycemic diabetic ketoacidosis: a potential complication of treatment with sodium-glucose cotransporter 2 inhibition. Diabetes Care. 2015;38(9):1687-1693.
Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(12):2739-2748.
Rewers A, Klingensmith G, Davis C, et al. Presence of diabetic ketoacidosis at diagnosis of diabetes mellitus in youth: the Search for Diabetes in Youth Study. Pediatrics. 2008;121(5):e1258-e1266.
Zisser H, Robinson L, Bevier W, et al. Bolus calculator: a review of four "smart" insulin pumps. Diabetes Technol Ther. 2008;10(6):441-444.
Lim Choi Keung SN, Arianayagam R, Soundararajan A, Donaghy M. Summary of the SADMANS mnemonic - a simple aide-memoire for drugs to pause or stop in acute kidney injury. Clin Med (Lond). 2020;20(6):e273-e274.
Goldenberg RM, Berard LD, Cheng AYY, et al. SGLT2 inhibitor-associated diabetic ketoacidosis: clinical review and recommendations for prevention and diagnosis. Clin Ther. 2016;38(12):2654-2664.
Salpeter SR, Greyber E, Pasternak GA, Salpeter EE. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010;(4):CD002967.
White M, Garbez R, Carroll M, Brinker E, Howie-Esquivel J. Is "teach-back" associated with knowledge retention and hospital readmission in hospitalized heart failure patients? J Cardiovasc Nurs. 2013;28(2):137-146.
Kessels RPC. Patients' memory for medical information. J R Soc Med. 2003;96(5):219-222.
Gómez AM, Henao Carrillo DC, Imitola Madero A, et al. Efficacy and safety of telehealth for the management of adults with type 1 diabetes during the COVID-19 pandemic. Diabetes Ther. 2021;12(2):439-449.
Fadini GP, de Kreutzenberg SV, Rigato M, et al. Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center. Diabetes Res Clin Pract. 2011;94(2):172-179.
Kamalakannan D, Baskar V, Barton DM, Abdu TAM. Diabetic ketoacidosis in pregnancy. Postgrad Med J. 2003;79(934):454-457.
Clore JN, Thurby-Hay L. Glucocorticoid-induced hyperglycemia. Endocr Pract. 2009;15(5):469-474.

Word Count: 2,000 words

Disclosure: No conflicts of interest to declare.

For Correspondence: Adapted for educational use in postgraduate medical training programs.

Search This Blog

Internal medicine