History

Fact Explanation
Polyuria, polydipsia and weight loss, Generally all of the glucose filtered by the kidneys are reabsorbed. When blood glucose reaches approximately 180 mg/dL, proximal tubular transport of glucose becomes saturated. The glucose remaining in the renal tubules travel into the distal nephron carrying water and electrolytes with it. This results in osmotic diuresis which is seen externally as polyuria. Hyperglycaemia and intravascular fluid depletion caused by polyuria results in a hyperosmolar state.Hyperosmolarity stimulates thirst mechanism. In type 2 diabetes since there is a relative insulin deficiency and /increased resistance to insulin peripheral uptake of glucose and storage is inhibited.This causes weight loss. [3][4][6]
Neurological symptoms such as drowsiness and lethargy, delirium,coma, focal or generalized seizures, visual changes or disturbances hemiparesis,sensory deficits If the renal fluid loss exceeds the normal body compensatory mechanisms,dehydration leads to hypovolemia which in turn, leads to hypotension, results in impaired tissue perfusion. Brain hypoxia and severe electrolyte imbalances(Na and K) due to hyperglycemia can cause these neurological symptoms. Hypoglycemia can result in low ATP production which could also cause these type of neurological symptoms. [5] [6][7]
Fever Since an underlying infection can precipitate a hyperglycemic episode. [3] [6]
History of carbohydrate rich meal. Since this could precipitate a hyperglycemic episode. [3][4]
History of type 1 diabetes mellitus(DM) Since Type 1 DM can precipitate an episode of diabetic ketoacidosis.[2]
History of type 2 DM Since type 2 DM can precipitate an episode of Hyperglycemia Hyperosmolar Nonketotic Coma (HONK) .[2]
Any history of discontinuation of hypoglycemic medications This could precipitate an episode of Diabetic Ketoacidosis (DKA) or HONK.[8]
Hunger Hypoglycemia can cause sympathoadrenal activation which result in hunger[3]
Nausea and vomiting, diffuse abdominal pain, decreased appetite, and anorexia In DKA due to acidosis and in hypoglycemia due to sympathoadrenal activation these symptoms occurs.[3]
Sweating Sympathoadrenal activation results in sweating in hypoglycaemia.[3]
References
  1. MATZ R. Management of the hyperosmolar hyperglycemic syndrome. Am Fam Physician [online] 1999 Oct 1, 60(5):1468-76 [viewed 19 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10524491
  2. GWINUP G, STEINBERG T. The management of diabetic coma. Calif Med [online] 1969 Nov, 111(5):347-350 [viewed 19 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1503677
  3. KEARNEY T, DANG C. Diabetic and endocrine emergencies. Postgraduate Medical Journal [online] 2007 February, 83(976):79-86 [viewed 19 May 2014] Available from: doi:10.1136/pgmj.2006.049445
  4. KITABCHI A. E., UMPIERREZ G. E., MILES J. M., FISHER J. N.. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care [online] December, 32(7):1335-1343 [viewed 19 May 2014] Available from: doi:10.2337/dc09-9032
  5. MCNAUGHTON C. D., SELF W. H., SLOVIS C.. Diabetes in the Emergency Department: Acute Care of Diabetes Patients. Clinical Diabetes [online] December, 29(2):51-59 [viewed 19 May 2014] Available from: doi:10.2337/diaclin.29.2.51
  6. Hyperglycemic Crises in Diabetes. Diabetes Care [online] 2004 January, 27(90001):94S-102 [viewed 19 May 2014] Available from: doi:10.2337/diacare.27.2007.S94
  7. UMPIERREZ G. E., MURPHY M. B., KITABCHI A. E.. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome. Diabetes Spectrum [online] 2002 January, 15(1):28-36 [viewed 19 May 2014] Available from: doi:10.2337/diaspect.15.1.28
  8. CHAITHONGDI N, SUBAUSTE JS, KOCH CA, GERACI SA. Diagnosis and management of hyperglycemic emergencies. Hormones (Athens) [online] 2011 Oct-Dec, 10(4):250-60 [viewed 21 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22281881

Examination

Fact Explanation
Dryness of the mucous membranes, anhidrosis, poor skin turgor, and sunken eyes Are signs of dehydration, caused by polyuria. [1]
Tachycardia In the early stages of dehydration although cardiac stroke volume decreases the heart rate increases to maintain a constant cardiac output. Hence, tachycardia will be one of the earliest signs of dehydration which is seen in hyperglycemic episodes. Sympathoadrenal activation results in tachycardia in hypoglycaemia. [1]
Hypotension With further volume loss, when the mean arterial pressure (MAP) longer can be maintained by increment of the peripheral resistance hypotension is seen. [1]
Neurological signs such as seizures, hemianopsia, aphasia, paresis, a positive Babinski sign, myoclonic jerks, change in muscle tone, nystagmus, eye deviation, and gastroparesis. During Hyperglycemia, cerebral dehydration, microvascular ischemia and changes in neurotransmitter level in the central nervous system may cause these signs. In hypoglycaemia low ATP production in the brain cells can cause similar signs [1]
Temperature-hyperthermia/hypothermia Sepsis suggested as an underlying cause by abnormally high or low temperature levels. Hypothermia is a poor prognostic factor. [1]
Tachypnoea (Kussmaul breathing)-rapid shallow breathing In DKA,to compensate for the metabolic acidosis respiratory rate is increased to remove the co2 to cause a respiratory alkalosis.
References
  1. Hyperglycemic Crises in Diabetes. Diabetes Care [online] 2004 January, 27(90001):94S-102 [viewed 19 May 2014] Available from: doi:10.2337/diacare.27.2007.S94

Differential Diagnoses

Fact Explanation
Diabetes insipidus This can present with polyuria,polydipsia and dehydration. [1]
These following conditions could cause altered mental status- central nervous system infection, hypoglycemia, hyponatremia, severe dehydration, uremia hyperammonemia, intoxication (eg, with ethanol, narcotics, other drugs), sepsis, postictal state, arrhythmia,hypotension, acute blood loss (gastrointestinal or other), excessive diuretic use All these, causes mental alteration and show neurological signs. [1]
Myocardial infarction Myocardial Infarction can precipitate DKA or HONK , therefore this diagnosis should also be considered. [1]
Pulmonary embolism Pulmonary embolism can also precipitate DKA or HONK ,therefore this diagnosis should also be considered. [1]
References
  1. GWINUP G, STEINBERG T. The management of diabetic coma. Calif Med [online] 1969 Nov, 111(5):347-350 [viewed 19 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1503677

Investigations - for Diagnosis

Fact Explanation
Plasma glucose This is an important investigation to differentiate between the three possibilel causes of a diabetic coma. A blood glucose level greater than 600 mg/dl is seen in HONK . In DKA blood glucose level is usually greater than 300 mg/dl In hypoglycaemia blood glucose level is less than 40 mg/dl. [1,2,3]
Serum ketones Small amount of ketones may be present in the serum in HONK. In DKA significant serum ketone concentration is present. [1,2,3]
Urine ketones by dipstick In DKA significant urinary ketones are present whereas in HONK small amount of ketones may be present in the urine. [1,2,]
Arterial blood gases In HONK Ph is greater than 7.30 whereas in DKA Ph is less than 7.3 causing a metabolic acidosis. [1,2,3]
Serum Osmolality Serum osmolarity is greater than 320mOsm/kg in HONK. In DKA serum osmolarity is greater than 290 mOsm/L (slightly less than HONK), but patients in coma with DKA typically have osmolalities greater than HONK (>330 mOsm/kg) . [1,2,3]
Electrolytes Hyponatremia is usually seen due to the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia. Hypernatremia in the presence of hyperglycemia indicates a profound degree of water loss. Hyperkalemia is seen due to an extracellular shift of potassium caused by insulin deficiency, hypertonicity, and acidemia. Bicarbonate level is greater than 15 mmol/l (>18Eeq/L )in HONK but is less than 15mmol/l in DKA.[1,2,3]
References
  1. Hyperglycemic Crises in Diabetes. Diabetes Care [online] 2004 January, 27(90001):94S-102 [viewed 19 May 2014] Available from: doi:10.2337/diacare.27.2007.S94
  2. MCNAUGHTON C. D., SELF W. H., SLOVIS C.. Diabetes in the Emergency Department: Acute Care of Diabetes Patients. Clinical Diabetes [online] December, 29(2):51-59 [viewed 19 May 2014] Available from: doi:10.2337/diaclin.29.2.51
  3. KEARNEY T, DANG C. Diabetic and endocrine emergencies Postgrad Med J [online] 2007 Feb, 83(976):79-86 [viewed 19 May 2014] Available from: doi:10.1136/pgmj.2006.049445

Investigations - Fitness for Management

Fact Explanation
Complete blood count with differential Hemoglobin and hematocrit values are usually elevated due to dehydration. Leukocytosis is frequently there, with white blood cell (WBC) counts exceeding 20,000/µL. Stress, dehydration, and demargination of leukocytes contribute to leukocytosis. Since infections commonly precipitate diabetic coma, leukocytosis should be considered secondary to an infectious process until proven otherwise. Therefore leucocyte count >25 000 mm3 is suggestive of an underlying bacterial infection. [1,2,3]
Bacterial cultures of urine, blood, and throat, etc. To find an infection as a precipitating cause for an hyperglycaemic episode. [1,2]
Electrocardiogram Patients suffering from a hyperglcaemic episode are considered to be having a silent MI (since MI is a precipitating factor)until proven otherwise therefore to detect ischemic changes electrocardiogram is done. Hypoglycaemia can also coexist with a MI.[1,2]
Chest x Ray To detect any chest infection as a precipitating cause for an hyperglycaemic episode chest X-Ray is done. [1,2]
Urinalysis To exclude any underlying urinary tract infection as a precipitating cause for a hypoglycaemic attack. [1,2]
References
  1. Hyperglycemic Crises in Diabetes. Diabetes Care [online] 2004 January, 27(90001):94S-102 [viewed 19 May 2014] Available from: doi:10.2337/diacare.27.2007.S94
  2. MCNAUGHTON C. D., SELF W. H., SLOVIS C.. Diabetes in the Emergency Department: Acute Care of Diabetes Patients. Clinical Diabetes [online] December, 29(2):51-59 [viewed 19 May 2014] Available from: doi:10.2337/diaclin.29.2.51
  3. KEARNEY T, DANG C. Diabetic and endocrine emergencies Postgrad Med J [online] 2007 Feb, 83(976):79-86 [viewed 19 May 2014] Available from: doi:10.1136/pgmj.2006.049445

Investigations - Followup

Fact Explanation
HbA1c To see the control of glucose level in the long term. This investigation is done 6 weekly. Preferably HbA1c level should be < 7% [1]
Fasting blood glucose/post prandial blood sugar level/random blood sugar level. To detect glycemic control in the short term. [1]
Urinary microalbumin level To detect any changes of early diabetic nephropathy. (30–299 mg/24 hr) [1]
Ophthalmological examination To detect diabetic retinopathy changes, annual eye examination is done. [1]
Lipid Profile Since diabetes increases the risk of cardiovascular disease,peripheral vascular disease and cerebrovascular accident by increasing atherosclerosis,this is screened by this investigation. [1]
References
  1. Standards of Medical Care in Diabetes--2014. Diabetes Care [online] December, 37(Supplement_1):S14-S80 [viewed 21 May 2014] Available from: doi:10.2337/dc14-S014

Management - General Measures

Fact Explanation
Initial management for unconscious patients. Protection of the airway is mandatory in obtund or unconscious patients.Oxygen is also given by face mask if hypoxic on air and if in respiratory failure by mechanical ventilation. Check the capillary blood glucose level and manage the hypoglycaemic or the hyperglycaemic episode appropriately. Nil by mouth (NBM) for at least 6 hrs and to prevent vomiting and aspiration NG tube is inserted.Urinary catheter is inserted if there is oligouria or high serum creatinine. [1,2]
Management of dehydration Initial fluid therapy is aimed toward expansion of the intravascular and extravascular volume and restoration of renal perfusion. In the absence of cardiac compromise, in HONK and DKA, initially 1L of 0.9% NaCl is infused during the first hour. Next 1L of N. saline is given every 2hrs for 4 hrs then 1L of N. saline is given every 6hrs until rehydrated for about 48 hrs. If the plasma Na is >160mmol/L, 0.45% may be given for the first 3L. Further fluid replacement is judged by the improvement in blood pressure, measurement of fluid input and output, laboratory values, and clinical examination. Fluid replacement should correct estimated deficits within the first 24 h. In patients with renal or cardiac compromise, monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid overload.[1,2]
Bicarbonate therapy Its not recommend to use unless the pH is <7. It can be given as 1.4% sodium bicarbonate 500 ml over 30 min, but it worsen the hypokalaemia.[1,2]
Phosphate replacement No clear benefit has been shown in the routine correction of hypophosphataemia using intravenous phosphate; it may actually be harmful, causing hypocalcaemia and hypomagnesaemia.If replacement is required, it is safer to use oral supplementation. [1,2]
Correcting hypokalemia. To prevent hypokalemia, potassium replacement is initiated after serum levels decrease to <5.3 mEq/l, assuming the presence of adequate urine output at 50 ml/h Generally, 20–30 mEq potassium in each liter of infusion fluid is sufficient to maintain a serum potassium concentration within the normal range of 4–5 mEq/l. Rarely, patients may present with significant hypokalemia. In such cases, potassium replacement should begin with fluid therapy, and insulin treatment should be delayed until potassium concentration is restored to >3.3 mEq/l to avoid arrhythmias or cardiac arrest and respiratory muscle weakness.[1,2]
References
  1. Hyperglycemic Crises in Diabetes. Diabetes Care [online] 2004 January, 27(90001):94S-102 [viewed 19 May 2014] Available from: doi:10.2337/diacare.27.2007.S94
  2. KEARNEY T, DANG C. Diabetic and endocrine emergencies Postgrad Med J [online] 2007 Feb, 83(976):79-86 [viewed 19 May 2014] Available from: doi:10.1136/pgmj.2006.049445

Management - Specific Treatments

Fact Explanation
Insulin Infusion Unless the episode of hyperglycaemic coma is uncomplicated and mild/moderate, regular insulin by continuous intravenous infusion is the treatment of choice. In adult patients, once hypokalemia (K+ < 3.3 mEq/l) is excluded, an intravenous bolus of regular insulin at 0.1 unit/kg body wt, followed by a continuous infusion of regular insulin at a dose of 0.1 unit · kg−1 · h−1 should be administered. This low dose of insulin usually decreases plasma glucose concentration at a rate of 50–75 mg · dl−1 · h−1 If plasma glucose does not decrease by 50–75 mg from the initial value in the first hour, the insulin infusion may be doubled every hour until a steady glucose decline is achieved. When the plasma glucose reaches 300 mg/dl in HONK and 250 mg/dl in DKA it may be possible to decrease the insulin infusion rate to 0.05–0.1 unit · kg−1 · h−1, at which time 5% dextrose may be added to the intravenous fluids. Thereafter, the rate of insulin administration or the concentration of dextrose may need to be adjusted to maintain the above-glucose values until mental obtundation and hyperosmolality are resolved. [1]
Subcutaneous insulin treatment Intravenous insulin infusion should be continued for 1–2 h after the subcutaneous insulin. Also, insulin infusion should not be stopped until patients are able to eat and drink normally. Patients with known diabetes can then be restarted on the current subcutaneous insulin regimen. In those newly diagnosed, a twice daily regimen using intermediate acting insulin is often used. The dose is split into two thirds given in the morning and one third in the evening. The dose of insulin is approximately 0.5–1.0 U/kg/day or to use the insulin requirement in the past 24 h on insulin infusion as a guide. The subcutaneous insulin needs to be started at least 1 h before the discontinuation of insulin infusion to avoid rebound hyperglycaemia. However, with the new rapid acting human insulin analogues (Aspart, Lispro and Glulisine), it may be possible to stop the insulin sliding scale immediately on starting subcutaneous insulin. Some patients with type 2 diabetes may be discharged on oral antiglycaemic agents.[1]
Treatment of hypoglycaemic episode In unconscious patients, friends or relatives trained in the use of glucagon can give 1 mg of glucagon intramuscularly or subcutaneously while awaiting medical help. Patients in hospital can be treated initially with 50 ml of 50% dextrose intravenous (via a large bore cannula) and glucagon, followed by 10% dextrose infusion. [1]
References
  1. KEARNEY T, DANG C. Diabetic and endocrine emergencies Postgrad Med J [online] 2007 Feb, 83(976):79-86 [viewed 19 May 2014] Available from: doi:10.1136/pgmj.2006.049445