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Indian Journal for the Practising Doctor

Clinical Update: Diabetic Emergencies

Author(s): Masoodi, S

Vol. 4, No. 6 (2008-01 - 2008-02)

Masoodi, S

ISSN: 0973-516X


Dr Shariq Masoodi, DM, is Additional Professor, Endocrinology Department, Sher-i-Kashmir Institute of Medical Sciences (SKIMS), Srinagar


The most severe and life threatening diabetic emergencies include: Diabetic ketoacidosis (DKA), HHS (HONK) and hypoglycemia.

Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis is a life-threatening emergency which occurs in most patients of Type 1 Diabetes. The complication may also arise in patients with type 2 dibetes mellitus due to progressive loss of β-cell reserve. Gross insulin deficiency is the predominant problem of DKA and mortality is ~5%–10%.

In Type 1 Diabetes Mellitus, the main hormonal pathophysiology is Insulin deficiency which results in decreased glucose utilization. This is accompanied with elevations in counter-regulatory hormones which lead to an increase of lipolysis in adipose tissue, proteolysis in muscle, glycogenolysis, gluconeogenesis, and hepatic ketogenesis leading to DKA.

Symptoms include blurred vision, increased thirst, increased urination, nausea/vomiting, confusion and subsequently loss of consciousness. Signs are dramatic with deep respirations, fruity breath, dehydration, hyperglycemia, ketosis and acidosis.

Lab criteria for DKA are:

  • Hyperglycemia ( glu>250 mg/dl)
  • Ketosis
  • Acidemia ( pH <7.3)
    • Bicarbonate <18 mmol/l

Hyperosmolar Hyperglycemic State (HHS)

Hyperosmolar Hyperglycemic State is another life-threatening emergency of diabeties. It occurs in patients with type 2 Diabetes Mellitus, and is characterized by very high blood glucose levels without ketones. Insulin secretion is maintained which prevents peripheral lipolysis and the liver is able to metabolize FFA in a nonketogenic manner.

In the USA, DKA occurs in 80% of whites, 53% of Blacks and 34% Hispanics with type 1 diabetes. In type 2 patients who develop DKA no precipitating factors may be evident. No difference in electrolytes, glucose, pH, arterial gases, plasma osmolality or level of ketosis is found in DKA whether complicating type 1 or type 2.

A relative insulin deficiency results in a decreased peripheral uptake of glucose and increased hepatic gluconeogenesis. There is a resultant hyperglycemia and hyperosmolality. Osmotic diuresis with a consequent volume and electrolyte depletion is present. Worth remembering is that DKA and HHS are not mutually exclusive.

Table 1. Comparison of Diabetic Emergencies

Feature Diabetic Ketoacidosis Hyperglycaemic non-ketotic coma
Diabetic history Known type I or new diabetic Mild or new type II diabetes
Age Young Old
Onset Days Days to weeks
Change in LOC o/+ ++
Acidosis +++ o/+
Fluid Loss ++ +++
Blood Sugar ++ +++

Table 2. Comparison of Diabetic Emergencies: Lab parameters

Constituent DKA HHS (HONK)
Glucose 250-600 600-1200
Sodium 125-135 135=145
Potassium Normal to increased Normal
Phosphorus Decreased Normal
Creatinine Slightly increased Moderately increased
Osmolaity 300-320 330-380
Plasma ketones ++++ +/-
Bicarbonate <15 mEq/l Normal to slightly increased
Arterial pH 6.8 – 7.3 >7.3
Anion gap 20 – 30 normal

Pathophysiology of DKA/HHS

Insulin Deficiency

Absolute insulin deficiency and concomitant overproduction of counter-regulatory hormones promote lipolysis. A shift in hepatic lipid metabolism of incoming fatty acids results due to high ratio of glucagon to insulin in portal flow, which in turn leads to a fall in malonyl Co A levels and dis-inhibition of CPT. Excess of CPT catalyzes the beta oxidative pathway- fatty acids are oxidized to form ketone bodies rather than reesterified into triglycerides.

Case Presentation

A 32 yr unmarried female with h/o type 1 DM, presents with nausea / vomiting and diffuse abdominal pain for the last 24 hours.

[What other questions would you like to ask?]

There is no h/o fever, upper respiratory symptoms, or urinary symptoms except for frequency.

The pt says that she has been using her insulin correctly, but she had not taken any insulin for the last 24 hours because she wasn’t able to eat anything.

She was diagnosed with DM after an episode of DKA ~= 7 years ago.

She is on insulin 70/30 28U (AM) + 16U(PM)

There is a family history of hypertension.
[What are pertinent findings on physical exam?]

Physical Exam

  • GPE: Mild distress but arousable, oriented
  • Vitals: 97.4, 120 (reg), 34, 132/88
  • Respiration: thoraco-abdominal, deep
  • CVS: tachycardia
  • Abd: (+) BS, diffuse tenderness, no rebound
  • Neuro: WNL

[What Lab Data would you like to obtain?]

Lab Data

  • Glucose- 612 mg/dl
  • WBC – 15.7, P75L25, Plt 250
  • NA 132, K 5.2, CL 96,
  • HCO 11
  • pH 7.15, HCO 11
  • BUN 10, Cr 1.0
  • Ca 12.1, P 6.6, Mg 2.1

[What is the actual serum sodium? What is the anion gap? What is the differential diagnosis for wide anion gap metabolic acidosis?]

  • UA: Protein 3+, ketones +++
  • Serum ketones were 1:16
  • Serum osmolarity was 323mOsm/kg (sOsm = 2 (Na + K ) + Glu/18 + BUN/2.8)
  • AG = Na – ( Cl + HCO3)
  • Na = Na + 1.6 x (Glu – 100)/100

insulin deficiency

Fig 1: Pathophysiology of DKA

Pathophysiology of DKA

Evaluation of patient

Diagnosis and evaluation of a patient of suspected Diabetes Ketoacidosis should include:

  • History of Diabetes Mellitus, medications and symptoms
  • History of complications
  • Utilization of medications
  • Social history ( including alcohol)
  • Vomiting
  • Precipitating factors – pregnancy, infection, omission of insulin, Myocardial infarction,, cardiovascular accident
  • Asses of hemodynamic status
  • Examination for presence of infection

Laboratory Evaluation

  • Glucose, urea, creat, electrolytes, CBC
  • Serum ketones
  • Calculate serum osmolality and AG
  • ABG
  • Urine analysis and culture
  • consider blood culture
  • CXR / ECG
  • HbA1c
  • measure serum osmolality if ingestion of osmotically active substance other than glucose suspected

Other expected labs in DKA

  • Hyponatermia unless pt is dehydrated
  • Hyperkalemia due to cellular shift
  • Leukocytosis in the absence of infection
  • Elevation of amylase and lipase in the absence of pancreatitis

“Euglycemic ketoacidosis”

  • Glu < 300 mg/dl
  • HCO3 < 10 mEq/l
  • Usually in pump pts (no “back-up insulin”)

Guidelines of therapy of DKA/HHS Treatment of DKA has 3 important pillars:

  • Give insulin in a sufficient amount
  • Monitor potassium status
  • Provide adequate hydration

a) Suggested Fluid Replacement in DKA/HHS

Administer normal saline as indicated below to maintain hemo-dynamic status than follow maintenance guidelines:

  • Normal saline for 1st 4 hours; consider ½ normal saline thereafter.
  • Change to D5 ½ NS when blood glucose reaches to < 259 mg/dl

The doctor may need to adjust the type and rate of fluid administration in the elderly and in patients with CHF and CRF.

Suggested fluid replacement in DKA /HHS

  • 1st hour : 1 L
  • 2nd hour : 1 L
  • 3rd hour : 0.5 – 1 L
  • 4th hour : 0.5 – 1 L
  • 5th hour : 0.5 – 1 L
  • Total 1st – 5th hour: 3.5 – 5 L
  • 6th – 12th hr : 250 – 500 ml/hr

Guidelines for Insulin Management in DKA/ HHS

  • Regular insulin 10U IV stat (for adults) or 0.15U/kg IV stat
  • Start regular insulin infusion 0.1 U/kg per hour or 5 U/ hr “Serum Ketone Negative DKA
  • Alcoholic ketoacidosis
  • Hypoxia
  • Beta hydroxybutirate is the dominant ketone
  • Not detected by nitroprusside reaction

Dose of insulin may be increased by 1 U/hr every 1-2 hours if <10 % drop in blood glucose or no improvement in acid - base status is evident.

Dose of insulin may be decreased by 1-2 U/hr when blood glucose < 250 mg/dl and/or progressive improvement in clinical status is seen with decrease in glucose >75 mg/dl /hr

Guidelines for Insulin Management in DKA/ HHS

  • Do not decrease insulin infusion to < 1 U/hr
  • Maintain blood gas between 140 - 180 mg/dl
  • If BG lt; 80 mg/dl, stop insulin infusion for no more than 1 hr and restart the infusion
  • If BG drops consistently to <100 mg/dl, change I.V. fluids to D-10 to maintain BG 140 – 180 mg/dl

Guidelines for K+ replacement in DKA/HHS

  • Don’t administer potassium if K+ < 5. 5 mEq/l or pt. is anuric
  • Use potassium chloride but alternate with potassium phosphate in severe phosphate depletion
  • Add IV K+ to each liter of fluid administered unless contraindicated

Table 3. Tailoring Potassium Dose to Serum Level

Serum K+ (mEq/L) Additional K reqd. (mEq/ L)
<3.5 40
3.5 – 4.5 20
4.5 – 5.5 10
>5.5 Stop K+ infusion

PROs of bicarbonate therapy:

  • severe acidosis is associated with adverese effects: hypotension, ↓ cardiac output, ↓ peripheral vascular resistance, pulmonary arterterial resistance, bardycardia, arrhytimas, renal and mesenteric ischemia, cerebral vasodilatation

CONS of bicarbonate therapy:

  • no studies have shown any benefit of bicarbonate if pH is 6.9-7.1
  • SIDE EFF : overshoot alkalosis, paradoxical CSF acidosis, hypokalemia, volume overload, overproduction of ketoacids

Guidelines for Bicarbonate Therapy in DKA

  • Use clinical judgement in deciding if bicarbonate therapy is indicated
  • If pH is < 7.0, consider 100 ml bicarbonate over 45 min (mix 100 ml sodium bicarbonate with 400 ml sterile water and administer at rate of 200 ml/hr)
  • Check arterial blood gases 30 min later

Phosphate replacement

Phosphate depletion is common in DKA; this is attributable to renal loss and intracellular uptake during insulin treatment.

Low cardiac output, respiratory muscle weakness, rhabdomyolisis, CNS deppression, seizures, coma, and renal failure are the complications of phosphate therapy. IV phosphate may lead to hypocalcemia.

No benefit has been shown by routine replacement; therefore, reserve phosphate replacement therapy if phosphate level < 1.5 mg/dl and in patients whose calcium level is normal.

Use of small amount of potassium phosphate and potassium chloride iv is safe and effective; however oral replacement is preferred to I.V.

Monitoring of Treatment

To avoid life-threatening complications, therapy of diabetic ketoacidosis should be monitored very closely. This includes:

  • Blood glucose hourly
  • Electrolytes and acid base status every 2-4 hours [It is fine to check venous pH if you can’t get arterial line ( 0.03 unit < arterial)]
  • Frequent measurements of ketones may be misleading (b hydroxybutyrate is converted to acetoacetate). [Consider bedside measurement of β hydroxybutyrate]
  • Repeat chest x-ray after 4 litre of fluid are administered

Complications of DKA Treatment

  • Hypoglycemia
  • Hypokalemia
  • Hypophosphatemia
  • Hyperchloremia and hyperchloremic acidosis – cl losses less severe than Na losses but replacement sols have equal part of Na and Cl
  • Hypoalcemia
  • Cerebral edema – children
  • MI
  • DVT / PE ( dehydration as a risk factor)

Hypoglycemia

Hypoglycemia is an ever present danger in diabetes and is considered “The greatest limiting factor in diabetes management“. In fact, 2-4% of the annual mortality associated with diabetes mellitus is attributable to hypoglycemia.

Primarily due to medications (antidiabetics, ethanol, other drugs), hypoglycemia can be caused by systemic diseases including endstage organ disease, sepsis, endocrine deficiencies and tumors.

Glucose is the obligate metabolic fuel for the brain. Since brain cannot synthesize glucose, it has to come from outside, and storage supply lasts only a few minutes. Glucose is transported across the blood brain barrier by facilitated diffusion; a decreased blood glucose leads to decreased transport. A delicate balance exists in the body to maintain a stable glucose level, liver being the pivot of this crucial balance.

Symptoms

Neuroglycopenic

  • Altered mental status
  • Confusion
  • Fatigue
  • Seizure
  • Loss of consciousness
  • Death

Neurogenic/Autonomic

  • Adrenergic
    • Palpitations
    • Tremor
    • Anxiety
  • Cholinergic
    • Diaphoresis
    • Hunger
    • Paresthesias

Definitions

  • “Mild“: Adrenergic (blood glucose<70)
  • “Moderate“: Cognitive (blood glucose<50)
  • “Severe“: Unconscious pt

Etiology of hypoglycemia

  • Diabetes Treatment
  • Reactive Hypoglycemia: Postprandial;
    [Patients undergone gastric surgery, with rapid transit into small bowel]
  • Fasting
    • Ethanol: blocks gluconeogenesis
    • Sepsis
    • Renal Failure: decreased insulin/antidiabetic medicine clearance
    • Endocrine deficiencies/Tumor
    • Medicine: Pentamidine, Quinine,
    • Salicylate, Sulfonamide, b-antagonists
    • Liver disease: critical illness due to ↓ endogenous glucose production
    • Factitious
  • Diabetes Associated hypo
  • Sulfonylurea (long acting)
  • Insulin Excess
    • Incorrect dosing/wrong timing/type ↓ Oral intake: illness, fasting glucose utilization: exercise sensitivity peripherally to insulin: wt loss, exercise
    • ↓ endogenous production
    • ↓ insulin clearance

Diagnosis of hypoglycemia depends on presence of Whipple’s Triad:

  • Symptoms suggestive of hypoglycemia
  • Low serum blood glucose
  • Relief of symptoms with normalization of blood glucose

Hypoglycemia Treatment

The diabetic patient should wear a card and also carry quick-carb foods with him, which may be sufficient for mild cases.

When blood glucose is severely low, the patient is unconscious / unresponsive and may have seizures.

Glucagon emergency kit

Glucagon emergency kit

Delayed Onset Hypoglycemia (DOH) may follow high-intensity exercise or extended duration activity. DOH may occur up to 24 hours after adjustments to food.

Prevention Strategies

Consistent monitoring of patient is required

  • Before All Meals and Snacks
  • Before and after exercise
  • At bedtime
  • At 3 a.m. (occasionally)

Caffeine

Caffeine helps reduce risk of nighttime hypolycemia, but not of daytime hypoglycemia. Benefit is seen with 4 cups of coffee per day (250 mg caffeine twice daily).

Target blood glucose levels in hypoglycemia

  • Pt is unable to recognize and verbalize lows: >80
  • Able to recognize and verbalize lows: >70
  • Pregnancy: >0
  • <10% of readings below target at each time of day
  • No severe lows

Further Reading:

  1. Arch Int Med 1999 159:2317
  2. Joslin’s Diabetes Mellitus 15th edition, 2005
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