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Transcript of Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Emergencies Author(s):...
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.