Project: Ghana Emergency Medicine Collaborative

Document Title: Diabetic Emergencies

Author(s): Andrew Wong (University of Michigan/St. Joseph Mercy Hospital), MD 2012

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3

Diabetic Emergencies

Andrew Wong, MDUniversity of Michigan/St. Joseph Mercy Hospital

Ann Arbor, MI, USA

4

ObjectivesPathophysiology of diabetes

Signs, symptoms, diagnosis and management of acute complications of diabetes: Hypoglycemia Diabetic ketoacidosis Hyperglycemic hyperosmolar nonketotic coma

5

Case 1 23yo F with history of DM Type I presents to the ED

for difficulty breathing.

7 days ago, she began having vaginal spotting, and dysuria

She lost her glucometer earlier this week and was unable to measure blood sugars

Today, she began to have nausea and vomiting and complained of abdominal pain.

Mother also noticed that she was having a hard time breathing

Found glucometer today and it read “high”

6

Case 1PMH: Type I DM

PSH: None

Medications: Cannot recall—uses both short acting and long-acting insulin

Allergies: None

SH: Sexually active; denies any illicit drug, alcohol or tobacco use. Senior in high school

7

Case 1 Physical Exam:

VS: T37 BP100/70 HR120 RR38 O2sat100%ra General: ill-looking thin female who appears to have labored

respirations HEENT: PERRL, EOMI, MM dry, OP clear Neck: soft, supple with no lymphadenopathy Lungs: CTAB, no w/r/r CV: tachycardic but regular rhythm, no m/r/r Abdomen: +BS. Diffusely tender with area of maximal

tenderness in the LLQ. No lesions found. No adnexal masses palpated

Pelvic: White creamy exhudate with +CMT and left adnexal tenderness

Extremities: cool to touch. 2+ radial, DP and posterior tibial pulses cap refill 3 seconds.

Skin: No rash, +skin tenting

8

Normal Physiology Glucose rise triggers pancreatic beta cells to release insulin

Insulin lowers serum glucose levels Stimulate glucose uptake and storage, facilitate use by fat and

muscle Inhibit glycogen breakdown in liver Degraded in 3-10 min in liver and kidney Inhibits hepatic gluconeogenesis and glycogenolysis Stimulate glycogen (stored form of glucose) storage

Fasting state stimulates pancreatic alpha cells to release glucagon Glucagon increases levels of glucose in blood

Stimulate liver to break down glycogen and release glucose Kidney release glucose in prolonged starvation Increases ketone production to enhance gluconeogenesis

9

BackgroundDiabetes

Most common endocrine disease Spectrum of disorders characterized by

hyperglycemia and disturbances in carbohydrate and lipid metabolism

Four types of DiabetesType I: Immune-mediated or idiopathic failure to

produce insulinType II: Hyperinsulinemic state due to resistance to

insulinGestational Diabetes Mellitis: during pregnancy;

similar to DMII Impaired Glucose Tolerance: increased risk of

developing DMII

10

EpidemiologyPrevalence of DM in US is 6.6%

5-10% have Type I 90-95% have Type II

Groups at risk for DM More in whites than nonwhites Native Americans

Age of onset Peak age of onset of Type I DM is 10-14years Onset of Type II DM tend to be older; younger

people getting disease due to obesity

11

Clinical FeaturesClinical Features Type I Diabetes Type II Diabetes

Body habitus Lean Obese

Age Younger than 40yo Middle-aged or older

Insulin levels Absent or low Normal to high

Onset Abrupt Gradual

Initial presentation of Type I DM usually DKA

Type II DM is being Dx in younger people

Diagnosis:

Any random plasma glucose >200mg/dL (11.1 mmol/dL) with symptoms of diabetes

Fasting plasma glucose >126mg/dL (7mmol/dL)

Plasma glucose >200mg/dL (11.1 mmol/dL) on 2 hour oral glucose tolerance test.

12

Hypoglycemia Background

Below 70 mg/dL (3.8mmol/dL), most symptomatic

Precipitants: Addison’s disease Akee fruit Anorexia nervosa Antimalarials Decrease in usual food

intake Ethanol Factitious hypoglycemia Hepatic impairment Hyperthyroidism Hypothyroidism Increase in usual exercise Insulin Islet cell tumors

Malfunctioning, improperly adjusted, or incorrectly used insulin pump

Malnutrution Old age Oral hypoglycemics Overaggressive treatment

of DKA or HHNC Pentamidine Phenylbutazone Propranolol Recent change of dose or

type of unsulin or oral hypoglycemic

Salicylates Sepsis Some antibacterial

sulfonylureas Worsening Renal

Insufficiency

13

HypoglycemiaBackground (cont’d)

Hypoglycemia unawareness Somogyi phenomenon

Signs and Symptoms Secondary to secretion of epinephrine and CNS

dysfunction Sweating, nervousness, tremor, tachycardia, hunger,

bizarre behavior, confusion, seizures, and coma.

Diagnostic Strategies Obtain blood glucose and other tests to find cause Factitious hypoglycemia: testing for insulin antibodies

and C peptide level

14

Oral hypoglycemic agents

Non hypoglycemic (taken individually) Biguanides (metformin)

decreases hepatic glucose production Alpha-Glucosidase inhibitors (acarbose, pioglitazone)

Decrease GI tract absorption of glucose Thiazolidinediones (rosiglitazone, pioglitazone)

Increase peripheral tissue glucose use

Hypoglycemic Insulin Sulfonylurea (i.e. glipizide)

Increases pancreatic insulin secretion Nonsulfonylurea secretagogues (repaglinide, nateglinide)

Increased pancreatic insulin secretion Glucagon-like peptide (Exanatide)

Stimulates release of insulin from pancreatic cells Dipeptidyl peptidase-4 inhibitors

Inhibits DPP-4 to prevent degredation of endogenous GLP

OsamaK, Wikimedia Commons

15

HypoglycemiaManagement

If patient is awake and cooperative, give sugar containing food or beverage PO

If unable to take PO25-75 gm glucose as D50W (1-3 amps) IVChildren: 0.5-1 g/kg glucose as D25W (2-4mL/kg)Neonates: 0.5-1 g/kg glucose (5-10mL/kg) as D10W

If unable to obtain IV access:1-2 mg glucagon IM or SQ; may repeat 20 min

Intropin, Wikimedia Commons

16

Diabetic KetoacidosisPathophysiology

Caused by cessation of insulin intake or by physical emotional stress

Source undetermined

17

Diabetic KetoacidosisClinical Features

Historyc/o polydipsia, polyuria, polyphagia, visual blurring,

weakness, weight loss, nausea, vomiting, and abdominal pain.

Seek reason for DKA Physical

Altered mental statusTachypnea with Kussmaul respirationsHypotension and other signs of dehydrationAcetone breath

18

Diabetic Ketoacidosis Diagnostic Strategies

Laboratory Tests Glucose: >350 mg/dL (19.4 mmol/dL)

Euglycemic DKA: 18% pts may have glucose less than 300 (16.6 mmol/dL)

Sodium: Low to normal Correct for hyperglycemia: 0.016 x (Glucose -100) High lipid content may cause falsely low levels.

Potassium: Normal to high Technically, potassium deficit due to K+ and H+ shifts Correct potassium for pH

(Serum potassium)-[0.6 (7.4-pH) x 10]

Acetoacetate and beta-hydroxybutyrate: elevated BUN and Cr: elevated

19

Diabetic Ketoacidosis Management

ABCs, IV, O2, Monitor Blood glucose, labs Dehydration

Fluids mainstay of therapy; pts usually down 3-5L Adult: 1-2L over 1-3 hrs; Child: 20 mL/kg over 1 hour Follow with fluid resuscitation to maintain UOP of 1-2mL/kg/hr

Insulin Infusion of 0.1 units/kg/hr up to 5-10 units/kg/hr Bolus of insulin prior to drip optional in adults;

contraindicated in children Check glucose every 1 hour Switch IV fluids to contain dextrose to prevent hypoglycemia

when BS 250-300 mg/dL (13.8-16.7 mmol/dL)

20

Diabetic KetoacidosisCorrect electrolyte abnormalities (check basic,

pH, ketones every 2 hours) Potassium

<4: 20mEq/hr 4-6: 10mEq/hr >6: none

MagnesiumSupplement 0.30 to 0.35 mEq/kg/day of magnesium

if deficient (1-3 grams in 70kg pt)

21

Diabetic KetoacidosisAcidosis

Bicarbonate may be indicated in pts pH ≤ 7.0 Usually not warranted

Worsen O2 release by shifting oxygen dissociation curve to left

Acidosis correction terminates Kussmaul respirations needed to get rid of CO2

Increases K+ requirementMay produce alkalosis which induces dysrhythmias

because of electrolyte shifts Inhibit feedback mechanism in which low pH inhibits

ketogenesisStudies show bicarbonate worsens prognosis in pts even

with pH as low as 6.9-7.1

22

Diabetic KetoacidosisComplications

Hypokalemia Hypoglycemia Alkalosis (from bicarb therapy) CHF Cerebral edema

Occurs 6-10 hrs after initiation of therapy and unless if glucose is below 250mg/dL (13.8 mmol/dL)

Consider if pt remains comatose or lapses into comaMortality 90%Use Mannitol 0.25-2 mg/kg

23

Diabetic KetoacidosisDisposition

Admit to hospital/ICU Consider outpatient if

Initial pH>7.35 Initial HCO3 ≥ 20 mEq/LCan tolerate PO fluidsSymptoms resolve in EDNo underlying precipitant requiring hospitalization

24

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC)

Background Characterized by hyperglycemia (38.8),

hyperosmolarity, dehydration, and altered mental status

Ketosis and acidosis are minimal or absent

Source undetermined

25

HHNCPathophysiology

Similar to DKA Absence of ketoacidosis is unknown

Theory: patients continue to secrete insulin to block ketogenesis.

Etiology More common in type II DM May occur in non diabetic pts (20% of

cases) especially after burns, hyperalimentation, peritoneal dialysis, or hemodialysis

Виталий Поспелов, Wikimedia Commons

26

HHNC Clinical Features

History Fever, thirst, polyuria, or oliguria Associated with chronic renal insufficiency, gram-negative PNA, GI

bleeding, gram-negative sepsis.

Physical Exam hypotension and other signs of dehydration Tachycardia Fever Altered mental status Seizures Signs of stroke Less commonly: choreoathetosis, ballismus, dysphagia, segmental

myoclonus, hemiparesis, hemianopsia, central hyperpyrexia, nystagmus, visual hallucinations, and acute quadriplegia

27

HHNCDiagnostic strategies

Laboratory TestingBlood glucose >600 mg/dL (33.3 mmol/dL)Serum osmolarity > 350 mOsm/LMay have metabolic acidosis 2/2 lactic acidosis,

starvation ketosisElectrolytes: decreased sodium, elevated potassium

28

HHNCManagement

DehydrationUsually 9L fluid deficit in a 70 kg pt2-3L of NS initially; may change to 0.45%NS

afterwardsSterile water to be considered concommitently for

pts with CHF Insulin Electrolytes

29

Case 1Work-up

30

Case 1 Laboratory results:

Na 134

K 7.0

Cl 106

HCO3 3

BuN 16

Cr 1.4

Glucose 770 (42.7)

Ca 9.4

Mg 2.6

Phos 7.3

WBC 6.2

Hbg 3.6

Hct 9.9

Plt 310

VBG pH 7.2

Wet Smear: + for clue cells

Urine Dip: +LE, Nitrite

Urine Micro 15-30wbc/hpf

31

Case 1EKG: Sinus tachycardia with normal axis,

intervals. +Peaked T waves in leads V1-6

CXR: no infiltrates

Pelvic Ultrasound: no acute abnormalities.

32

Case 1Hospital course

Started on IV fluids, Insulin drip Started on Flagyl, Cefotetan, Doxycycline Blood and urine cultures were positive for E. coli

33

SourcesMarx J. Rosen’s Emergency Medicine, 7th Ed,

2009.

Rucker D. “Diabetic Ketoacidosis.” eMedicine Emergency Medicine, 4 Jun 2010.