GEMC- Diabetic Emergencies- Resident Training
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Transcript of GEMC- Diabetic Emergencies- Resident Training
Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Emergencies Author(s): Andrew Wong (University of Michigan/St. Joseph Mercy Hospital), MD 2012 License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/
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Objectives � Pathophysiology of diabetes
� Signs, symptoms, diagnosis and management of acute complications of diabetes: � Hypoglycemia � Diabetic ketoacidosis � Hyperglycemic hyperosmolar nonketotic coma
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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”
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Case 1 � PMH: 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
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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
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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
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Background � Diabetes
� Most common endocrine disease
� Spectrum of disorders characterized by hyperglycemia and disturbances in carbohydrate and lipid metabolism
� Four types of Diabetes � Type I: Immune-‐mediated or idiopathic failure to produce insulin
� Type II: Hyperinsulinemic state due to resistance to insulin
� Gestational Diabetes Mellitis: during pregnancy; similar to DMII
� Impaired Glucose Tolerance: increased risk of developing DMII
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Epidemiology � Prevalence 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
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Clinical Features Clinical 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.
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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
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Hypoglycemia � Background (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
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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
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OsamaK, Wikimedia Commons
Hypoglycemia � Management
� If patient is awake and cooperative, give sugar containing food or beverage PO
� If unable to take PO � 25-‐75 gm glucose as D50W (1-‐3 amps) IV
� Children: 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
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Intropin, Wikimedia Commons
Diabetic Ketoacidosis � Pathophysiology
� Caused by cessation of insulin intake or by physical emotional stress
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Source undetermined
Diabetic Ketoacidosis � Clinical Features
� History � c/o polydipsia, polyuria, polyphagia, visual blurring, weakness,
weight loss, nausea, vomiting, and abdominal pain.
� Seek reason for DKA � Physical
� Altered mental status
� Tachypnea with Kussmaul respirations
� Hypotension and other signs of dehydration � Acetone breath
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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
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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)
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Diabetic Ketoacidosis � Correct electrolyte abnormalities (check basic, pH,
ketones every 2 hours) � Potassium
� <4: 20mEq/hr
� 4-‐6: 10mEq/hr
� >6: none
� Magnesium � Supplement 0.30 to 0.35 mEq/kg/day of magnesium if deficient
(1-‐3 grams in 70kg pt)
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Diabetic Ketoacidosis � Acidosis
� 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+ requirement � May produce alkalosis which induces dysrhythmias because of
electrolyte shifts � Inhibit feedback mechanism in which low pH inhibits
ketogenesis � Studies show bicarbonate worsens prognosis in pts even with
pH as low as 6.9-‐7.1
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Diabetic Ketoacidosis � Complications
� 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 coma
� Mortality 90%
� Use Mannitol 0.25-‐2 mg/kg
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Diabetic Ketoacidosis � Disposition
� Admit to hospital/ICU
� Consider outpatient if � Initial pH>7.35 � Initial HCO3 ≥ 20 mEq/L
� Can tolerate PO fluids
� Symptoms resolve in ED
� No underlying precipitant requiring hospitalization
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Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC)
� Background � Characterized by hyperglycemia (38.8), hyperosmolarity,
dehydration, and altered mental status � Ketosis and acidosis are minimal or absent
24 Source undetermined
HHNC � Pathophysiology
� 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
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Виталий Поспелов, Wikimedia Commons
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
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HHNC � Diagnostic strategies
� Laboratory Testing � Blood glucose >600 mg/dL (33.3 mmol/dL)
� Serum osmolarity > 350 mOsm/L
� May have metabolic acidosis 2/2 lactic acidosis, starvation ketosis
� Electrolytes: decreased sodium, elevated potassium
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HHNC � Management
� Dehydration � Usually 9L fluid deficit in a 70 kg pt � 2-‐3L of NS initially; may change to 0.45%NS afterwards
� Sterile water to be considered concommitently for pts with CHF
� Insulin � Electrolytes
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Case 1 � Work-‐up
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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
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Case 1 � EKG: Sinus tachycardia with normal axis, intervals.
+Peaked T waves in leads V1-‐6
� CXR: no infiltrates
� Pelvic Ultrasound: no acute abnormalities.
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Case 1 � Hospital course
� Started on IV fluids, Insulin drip � Started on Flagyl, Cefotetan, Doxycycline � Blood and urine cultures were positive for E. coli
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Sources Marx J. Rosen’s Emergency Medicine, 7th Ed, 2009.
Rucker D. “Diabetic Ketoacidosis.” eMedicine Emergency Medicine, 4 Jun 2010.
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