Starvation KetosisMANAGEMENT

ENDOCRINE AND METABOLIC PRESENTATIONS · 12 SECTIONS

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705 items

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

Acute Porphyria Adrenal crisis Adrenal Insufficiency (Addisonian Crisis)Dehydration Diabetes Insipidus Diabetic Ketoacidosis (DKA)Euglycemic DKA (SGLT2 inhibitor)Galactosemia GLP-1 receptor agonist complications (retained gastric contents, aspiration risk)Homocystinuria Hypercalcemia Hyperkalemia Hypermagnesemia Hypernatremia Hyperosmolar Hyperglycemic State (HHS)Hypertensive emergency Hypertensive urgency Hypocalcemia Hypoglycemia Hypogonadism (Acute Presentation)Hypokalemia Hypomagnesemia Hyponatremia Hypoparathyroidism (Tetany)Insulin pump failure Maple Syrup Urine Disease (Crisis)Medium-Chain Acyl-CoA Dehydrogenase Deficiency (MCAD)Metabolic Acidosis Metabolic Alkalosis Myasthenia gravis crisis Myxedema coma Pellagra Pheochromocytoma (Crisis)Pituitary Apoplexy Pompe Disease (GSD II)Respiratory Acidosis Respiratory Alkalosis Scurvy SIADH Starvation Ketosis Tarui Disease (GSD VII)Thyroid storm Tyrosinemia Vitamin D Deficiency (Severe-Rickets)Von Gierke Disease (GSD I)

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp60

Immediate priorities

›Airway and breathing threats

›Kussmaul respirations indicating significant acidemia

›Deep labored breathing pattern

›pH < 7.1 possible in pregnancy or concurrent illness

›Altered mental status

›Confusion or obtundation from severe acidosis

›Hypoglycemia contributing to encephalopathy

›If GCS < 13 or unable to protect airway, escalate to resuscitation bay

›Rapid sequence intubation preparation

›Endocrinology or critical care consultation

›Circulation threats

›Hemodynamic instability from dehydration

›Tachycardia

›Hypotension SBP < 90 mmHg

›Hypoglycemia as life threat

›Point-of-care glucose immediately

›Pediatric and pregnant patients at highest risk

›If glucose < 3.0 mmol/l, IV dextrose immediately

›D10W 250 ml IV bolus in adults

›D25W 2 ml/kg IV in pediatric patients

›Key early branching

›Starvation ketosis spectrum

›Mild ketosis: pH > 7.3, bicarbonate > 18 mmol/l

›Starvation ketoacidosis: pH < 7.3, high anion gap

›Exclude DKA, alcoholic ketoacidosis, SGLT2i-related euglycemic DKA

›Glucose level, alcohol history, medication review

›Anion gap calculation

02History/hx76

Presentation pattern

›Core symptoms

›Nausea and vomiting

›Duration and frequency

›Onset relative to reduced oral intake

›Weakness and malaise

›Progressive over days of poor intake

›Lethargy and decreased activity

›Abdominal pain

›Ketoacidosis can mimic surgical abdomen

›Diffuse or epigastric pattern

›Respiratory symptoms

›Dyspnea or rapid breathing

›Kussmaul pattern suggesting acidemia

›Distinguish from cardiac or pulmonary cause

›Fruity or acetone breath

›Acetoacetate volatile excretion

›Classic but not always present

Intake and fasting history

›Duration and degree of oral restriction

›Days of fasting or near-fasting

›24 to 48 hours sufficient in pregnancy or children

›5 to 7 days for significant ketosis in healthy adults

›Caloric content of recent intake

›Carbohydrate restriction specifically

›Ketogenic diet history

›Reason for poor intake

›Vomiting from any cause

›Psychiatric illness, depression, psychosis, eating disorder

›Post-bariatric surgery intolerance

›Abdominal pathology

›Important negatives

›Diabetes history

›Type 1 increases DKA risk

›Type 2 increases euglycemic DKA risk with SGLT2 inhibitors

›Alcohol use history

›Chronic use and recent binge-cessation pattern

›Alcoholic ketoacidosis overlap common

›SGLT2 inhibitor use

›Empagliflozin, dapagliflozin, canagliflozin

›Euglycemic DKA triggered by starvation plus SGLT2 inhibitor

Risk factors

›High-risk populations

›Pregnancy especially third trimester

›Accelerated starvation physiology from placental hormones

›Even 12 to 24 hours of fasting can precipitate severe ketoacidosis

›Eating disorders

›Anorexia nervosa and bulimia nervosa

›Chronic restriction with episodic restriction and purging

›Pediatric patients under age 10

›Intercurrent illness with vomiting and reduced intake

›Below 50th percentile for weight increases risk

›Comorbid contributors

›Chronic alcohol use

›Reduced glycogen stores

›AKA and starvation ketosis frequently coexist

›Post-bariatric surgery

›Sleeve gastrectomy and gastric bypass reduce tolerance

›Perioperative and early recovery period highest risk

›Chronic liver disease

›Impaired gluconeogenesis and reduced glycogen stores

›Faster depletion of glucose reserves during fasting

›Hyperemesis gravidarum or gastroparesis

›Prolonged vomiting causing starvation state

›Thiamine depletion risk concurrent

Social and collateral history

›Collateral history often essential

›Psychiatric patients may not provide accurate dietary history

›Confirm intake with family, caregivers, nursing staff

›Food refusal in catatonia, psychosis, depression

›Social determinants

›Homelessness and food insecurity

›Social isolation and neglect

›Family history

›Diabetes mellitus to exclude DKA

›Type 1 in first-degree relatives

›Autoimmune disease history

›Inborn errors of metabolism in pediatric cases

›Fatty acid oxidation disorders

›Recurrent ketotic episodes

03Physical Exam/exam61

Vitals and general

›Vital sign pattern

›Tachycardia from dehydration and acidosis

›HR > 100 bpm as early marker

›Severity correlates with volume depletion

›Tachypnea

›Kussmaul respirations compensating for metabolic acidosis

›RR > 25 per minute in significant acidemia

›Hypotension in severe volume depletion

›SBP < 90 mmHg as critical threshold

›Orthostatic changes in moderate dehydration

›Hypothermia in severe malnutrition or chronic starvation

›Reduced metabolic rate

›Adrenal insufficiency overlap consideration

›General appearance

›Cachectic or malnourished habitus

›Temporal wasting

›Loss of subcutaneous fat

›Fruity or acetone odor on breath

›Acetoacetate volatilization

›Not reliably absent even with significant ketosis

Focused examination

›Hydration and perfusion

›Dry mucous membranes

›Lips and tongue assessment

›Sunken eyes in moderate dehydration

›Skin turgor

›Tenting on dorsum of hand

04Differential Diagnosis/ddx45

Ketoacidotic states

›Diabetic ketoacidosis

›ICD-10 E11.10 type 2 without coma, E10.10 type 1

›Glucose typically > 14 mmol/l

›Euglycemic DKA exception with SGLT2 inhibitors

›Absolute insulin deficiency mechanism

›History of diabetes distinguishes from pure starvation

›Alcoholic ketoacidosis

›ICD-10 E51.8 thiamine and metabolic context

›Binge drinking followed by cessation and vomiting

›Low-normal glucose characteristic

›Elevated NADH/NAD ratio shifts to beta-hydroxybutyrate predominance

›Frequently coexists with starvation ketosis

›SGLT2 inhibitor-related euglycemic DKA

›ICD-10 E13.10 applicable

›Normal or near-normal glucose despite significant ketosis

›SGLT2 inhibitor use plus reduced carbohydrate intake trigger

›May recur after initial resolution

Toxic and metabolic causes of high anion gap

›Lactic acidosis

›Elevated lactate > 2 mmol/l

›Sepsis, shock, metformin toxicity, liver failure

›Lactate is key differentiating lab

›ICD-10 E87.2 acidosis

›Toxic alcohol ingestion

›Methanol and ethylene glycol

›Elevated osmolar gap

›Specific toxidromes and target organ effects

05Laboratory Tests/lt64

Core metabolic panel

›Point-of-care glucose

›Typically normal or low in starvation ketosis

›Normal distinguishes from classic DKA

›< 3.0 mmol/l constitutes hypoglycemia requiring immediate treatment

›Repeat every 1 to 2 hours during treatment

›Target 5 to 10 mmol/l during dextrose infusion

›Avoid overcorrection causing hyperglycemia

›Anion gap calculation

›Na - (Cl + bicarbonate) normal < 12 mmol/l

›Elevated in ketoacidosis, lactic acidosis, toxic ingestions

›Delta-delta ratio to identify mixed disorders

›ACEP Level B recommendation to calculate anion gap in any suspected metabolic acidosis

›Electrolytes

›Sodium

›Pseudohyponatremia with severe ketosis less common than DKA

›True hyponatremia from vomiting losses

›Potassium

›May be normal or low with vomiting

›Repletion before aggressive insulin therapy if DKA overlap

›Bicarbonate

›< 18 mmol/l suggests metabolic acidosis

›Trend is key treatment response indicator

Ketone and acid-base markers

›Beta-hydroxybutyrate serum level

›Most reliable ketone marker

›>= 2.5 mmol/l indicates clinically significant ketosis

›Can reach 2.5 to 4.5 mmol/l after 5 to 7 days of fasting

06Diagnostic Tests/dt69

Scoring Systems

›Ketoacidosis severity assessment

›Mild starvation ketoacidosis

›pH 7.25 to 7.30

›Bicarbonate 15 to 18 mmol/l

›Beta-hydroxybutyrate 2.5 to 4.5 mmol/l

›Moderate starvation ketoacidosis

›pH 7.10 to 7.25

›Bicarbonate 10 to 15 mmol/l

›Hemodynamic instability or altered mental status

›Severe starvation ketoacidosis

›pH < 7.10

›Bicarbonate < 10 mmol/l

›Altered consciousness or hemodynamic compromise

›Refeeding syndrome risk stratification using NICE criteria

›High risk features

›BMI < 16 kg/m2

›Weight loss > 15% in past 3 to 6 months

›Little or no nutritional intake for > 10 days

›Low phosphate, potassium, or magnesium before refeeding

›Very high risk features

›BMI < 14 kg/m2

›Weight loss > 20% in past 3 to 6 months

›Negligible intake for > 2 weeks

MRI

›MRI role in starvation ketosis

›Limited routine acute utility

›Not indicated for diagnosis of ketosis

07Disposition/dispo44

Admission indications

›Hospital admission criteria

›Significant acidosis

›pH < 7.30 or bicarbonate < 15 mmol/l

›Anion gap elevation

›Hemodynamic instability

›Tachycardia > 120 bpm not improving with initial fluids

›Hypotension SBP < 90 mmHg

›Altered mental status

›Confusion or obtundation

›Inability to take oral fluids safely

›High-risk population

›All pregnant patients with starvation ketoacidosis

›Pediatric patients with ketoacidosis

›Eating disorder patients requiring monitoring

›ICU admission criteria

›Severe acidemia pH < 7.10

›Mechanical ventilation consideration

›Intensive monitoring required

›Hemodynamic instability requiring vasopressors

›Norepinephrine infusion

›Central venous access

›Altered consciousness with airway risk

›Intubation and ventilatory support

›Neurological monitoring

Discharge criteria

›Criteria for discharge

›Resolution of ketoacidosis

08Treatment/t80

Carbohydrate repletion

›Dextrose-containing IV fluids as cornerstone

›Mild ketosis with ability to tolerate oral intake

›Oral carbohydrates first line

›Juice, crackers, carbohydrate-containing foods

›Resolution within hours expected

›Moderate to severe ketosis or inability to tolerate PO

›D5 0.9% NaCl (D5NS) or D5 0.45% NaCl (D5 half-normal saline)

›125 to 250 ml per hour rate titrated to glucose target

›Hypoglycemia present

›D10W 250 ml IV bolus in adults

›D25W 2 ml/kg IV for pediatric patients

›Recheck glucose 15 to 30 minutes after bolus

›Insulin considerations

›Generally not required in pure starvation ketosis

›Endogenous insulin response adequate with carbohydrate administration

›Insulin increases risk of hypoglycemia

›Insulin only if concurrent DKA confirmed

›Regular insulin 0.1 units/kg/hour infusion for DKA

›Monitor potassium before initiating insulin

Fluid resuscitation

›Volume replacement strategy

›Isotonic crystalloid for hemodynamic instability

›Normal saline or lactated Ringer's 500 ml to 1 L bolus

›Reassess hemodynamic response after each bolus

›Transition to dextrose-containing fluids once volume restored

›D5NS at maintenance plus ongoing losses

›Avoid prolonged free water restriction

›Potassium supplementation

›Potassium < 3.5 mmol/l requires replacement before insulin

›KCl 20 to 40 mmol/l added to IV fluid

›Cardiac monitoring during rapid repletion

Thiamine and micronutrient repletion

›Thiamine administration

›100 mg IV before dextrose in any patient at risk for Wernicke encephalopathy

›Chronic alcohol use history

›Prolonged starvation or eating disorder

›Clinical Medicine 2020 recommendation

›Mechanism of risk

›Dextrose administration accelerates thiamine consumption

›Wernicke encephalopathy precipitated by glucose loading without thiamine

›Prophylactic thiamine for all moderate to severe starvation ketosis cases

›100 mg IV thiamine before first dextrose dose

›Continue daily until adequate oral intake achieved

›Electrolyte repletion

›Phosphate monitoring and repletion

›Hypophosphatemia develops with refeeding

›Sodium phosphate 0.3 mmol/kg IV over 6 hours for moderate depletion

›Magnesium

›Deficiency common in chronic malnutrition

›Magnesium sulfate 2 g IV over 4 to 6 hours for symptomatic deficiency

›Multivitamin infusion

›Especially if prolonged starvation

›B-complex vitamins in IV fluids

Refeeding syndrome prevention

›Risk identification

›NICE high-risk criteria assessment

›BMI < 16 or > 20% weight loss

›Minimal intake > 5 days

›Pre-existing electrolyte abnormalities

›ASPEN 2020 consensus recommendations

›Start nutrition at 50% of estimated caloric goal

›Advance over 4 to 7 days in high-risk patients

›Monitoring during refeeding

›Electrolytes every 6 to 12 hours initially

›Phosphate, potassium, magnesium

›Correct deficiencies promptly

›Fluid balance monitoring

›Avoid fluid overload from edema shifts

›Daily weights when admitted

›Caloric prescription

›High-risk patients start at 10 to 20 kcal/kg/day maximum

›Advance by 200 to 400 kcal per day

›Target 25 to 30 kcal/kg/day over 5 to 7 days

›Carbohydrate emphasis initially

›Glucose substrate stops ketogenesis

›Protein introduction gradual

SGLT2 inhibitor management

›Sick-day rules for SGLT2 inhibitor patients

›Hold SGLT2 inhibitor during illness, fasting, or perioperative periods

›Emergency Medicine Australasia 2020 guidance

›Resume only after adequate oral intake restored

›Do not restart until ketosis resolved and eating normally

›Confirm beta-hydroxybutyrate normalized

›Communicate with prescribing physician

09Special Populations/sp83

Pregnancy

›Accelerated starvation physiology

›Physiologic basis

›Placental hormones including human placental lactogen create relative insulin resistance

›Glucagon secretion augmented in late pregnancy

›Even 12 to 24 hours of fasting can precipitate severe ketoacidosis

›Clinical presentation

›Hyperemesis gravidarum common precipitant

›Severity disproportionate to duration of fasting

›pH < 7.1 reported in non-diabetic pregnant women

›Management in pregnancy

›Obstetrics consultation immediately for any pregnant patient with ketoacidosis

›Fetal monitoring when gestational age > 24 weeks

›Non-reassuring fetal heart rate may improve with maternal acidosis correction

›IV dextrose-containing fluids same cornerstone as non-pregnant adults

›D5NS preferred to avoid excessive sodium

›Thiamine 100 mg IV before dextrose

›Antiemetics for hyperemesis

›Ondansetron 4 mg IV for refractory vomiting

›Metoclopramide 10 mg IV alternative

›Avoid prolonged fasting post-discharge

›Small frequent carbohydrate-containing meals

›Maximum 12-hour fasting interval

›Fetal considerations

›Fetal ketone exposure

›Crosses placenta and may affect neurological development

›Rapid maternal treatment is fetal treatment

›Emergent delivery consideration if fetus compromised and gestational age allows

›Rare indication

›Maternal stabilization usually sufficient

Geriatric

›Atypical presentations in older adults

›Clinical features

›Delirium may be primary presenting symptom

›Weakness and falls without prominent GI symptoms

›Hypothermia more common than fever

›Contributing factors

›Social isolation and food insecurity

›Polypharmacy reducing appetite

›Dysphagia from neurological disease

›Management modifications in elderly

›Fluid resuscitation caution

›Reduced cardiac reserve increases pulmonary edema risk

›250 ml boluses with reassessment rather than 1 L bolus

›Furosemide available at bedside

›Renal dosing adjustments

›eGFR-based fluid and electrolyte replacement calculations

›Avoid hyperkalemia with aggressive potassium repletion

›Cognitive baseline assessment

›Delirium overlying dementia common

›Capacity assessment for nutritional decisions

›Disposition considerations for elderly

›Lower threshold for admission

›Limited functional reserve

›Home safety concerns with reduced oral intake

›Social work and home care planning

›Meal support services

›Follow-up nutritional monitoring

Pediatrics

›Pediatric vulnerability

›Higher risk of rapid deterioration

›Children under 10 years at highest risk

›Smaller glycogen stores deplete faster

›Intercurrent illness with vomiting common trigger

›Prevalence data

›Pediatric Emergency Care 2022 prospective study estimates clinically significant prevalence in children presenting with vomiting and reduced intake

›Those below 50th percentile for weight have higher risk

›Pediatric clinical features

›Vomiting and lethargy most common presenting symptoms

›Seizures from ketotic hypoglycemia

›Rapid breathing from acidosis compensation

›Fruity breath may be noted by caregivers

›Pediatric management

›Hypoglycemia treatment

›D25W 2 ml/kg IV bolus for glucose < 3.0 mmol/l

›D10W 2.5 ml/kg IV bolus as alternative

›Maintenance D10W at 1.5 times maintenance rate

›Oral carbohydrates if tolerating

›Juice 100 ml for child over 2 years

›Advance to crackers and complex carbohydrates when tolerating

›Thiamine 25 to 50 mg IV in children with prolonged starvation or alcohol exposure

›Weight-based dosing 0.5 to 1 mg/kg IV

›Pediatric disposition

›Lower threshold for admission

›Ensure adequate home monitoring and feeding plan before discharge

›Pediatric or family medicine follow-up within 24 hours

10Background/b64

Epidemiology

›Population data

›Underrecognized condition across all age groups

›Frequently misdiagnosed as DKA or AKA

›Psychiatric and bariatric surgical populations at elevated risk

›Specific high-risk groups

›Eating disorders affect 9% of global population with significant starvation ketosis risk

›Post-bariatric surgery patients at increased risk in perioperative period

›Pregnant women particularly susceptible to accelerated starvation ketosis

›Pediatric prevalence

›Pediatric Emergency Care 2022 prospective study documented significant prevalence in ED presentations with vomiting and reduced intake

›Children under 10 years with weight below 50th percentile highest risk subgroup

Pathophysiology

›Metabolic cascade of starvation

›Glycogen depletion phase

›Hepatic glycogen exhausted within 12 to 24 hours of fasting in most adults

›Faster in pregnant women, children, and those with liver disease

›Blood glucose begins to fall

›Hormonal adaptation

›Insulin falls as glucose drops

›Glucagon rises driving gluconeogenesis

›Counter-regulatory hormones activate lipolysis

›Ketogenesis

›Fatty acids mobilized from adipose tissue

›Beta-oxidation in liver mitochondria produces acetyl-CoA

›Acetyl-CoA converted to beta-hydroxybutyrate and acetoacetate

›Ketone body metabolism and acid-base effects

›Normally mild acidosis only

11Patient Discharge Instructions/pdi37

copy discharge instructions

›What happened

›Starvation ketosis: your body ran low on carbohydrates and began burning fat for energy, making your blood more acidic

›This resolves with carbohydrate intake and fluids

›Full recovery expected when eating normally

›What to eat and drink at home

›Regular meals with carbohydrate-containing foods

›Bread, rice, pasta, crackers, fruit, juice

›Do not skip meals especially when unwell

›Stay well hydrated

›Water, juice, sports drinks

›Small sips frequently if nauseous

›Avoid prolonged fasting

›Maximum fast overnight

›If vomiting prevents eating, seek care early

›Medications at home

›If prescribed SGLT2 inhibitor (eg. empagliflozin, dapagliflozin, canagliflozin)

›Hold this medication when unwell, fasting, or not eating normally

›Restart only when eating and drinking normally and confirmed with your doctor

›Take any vitamins or supplements as prescribed

›Thiamine if prescribed

›Multivitamins

›Warning signs to return to emergency immediately

›Confusion, difficulty thinking clearly, or unusual sleepiness

›Fruity smell on breath returning

›Unable to keep any fluids or food down for more than 4 to 6 hours

›Rapid or labored breathing

›Blood sugar < 4 mmol/l on home monitor

12References/r22

Guidelines and key sources

›Primary evidence sources

›Gall AJ, Duncan R, Badshah A. Starvation Ketoacidosis on the Acute Medical Take. Clinical Medicine. 2020. PMID 32414718

›Clinical presentation, management, thiamine recommendation

›Frise CJ, Mackillop L, Joash K, Williamson C. Starvation Ketoacidosis in Pregnancy. European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2013. PMID 23131345

›Pregnancy-specific accelerated starvation physiology

›Millar R, Chiappazzo A, Palmer B. Starvation Ketosis in the Pediatric Emergency Department. Pediatric Emergency Care. 2022. PMID 33170568

›Pediatric prevalence and risk stratification

›Supporting references

›Bashir B, Fahmy AA, Raza F, Banerjee M. Non-Diabetic Ketoacidosis: A Case Series and Literature Review. Postgraduate Medical Journal. 2021. PMID 33246966

›Spectrum of non-diabetic ketoacidosis presentations

›da Silva JSV, Seres DS, Sabino K, et al. ASPEN Consensus Recommendations for Refeeding Syndrome. Nutrition in Clinical Practice. 2020

›Refeeding syndrome prevention and management

›Morton A. Ketoacidosis in the Emergency Department. Emergency Medicine Australasia. 2020. PMID 32266781

›SGLT2 inhibitor sick-day rules and ketoacidosis spectrum

›Palmer BF, Clegg DJ. Starvation Ketosis and the Kidney. American Journal of Nephrology. 2021. PMID 34350876

›Renal handling of ketones and acid-base physiology

›Kamel KS, Halperin ML. Acid-Base Problems in Diabetic Ketoacidosis. New England Journal of Medicine. 2015

›Ketoacidosis acid-base physiology applicable to starvation context

›Treasure J, Duarte TA, Schmidt U. Eating Disorders. Lancet. 2020. PMID 32171414

›Eating disorder epidemiology and clinical features

›Long B, Lentz S, Koyfman A, Gottlieb M. Euglycemic Diabetic Ketoacidosis. American Journal of Emergency Medicine. 2021. PMID 33626481

›SGLT2 inhibitor euglycemic DKA and starvation overlap

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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