Current Medical Issues

PRACTICE GUIDELINES
Year
: 2017  |  Volume : 15  |  Issue : 3  |  Page : 208--210

Hyperglycemic diabetic emergencies: Practice guidelines


Kundavaram Paul Prabhakar Abhilash 
 Department of Accident and Emergency Medicine, Christian Medical College, Vellore, Tamil Nadu, India

Correspondence Address:
Kundavaram Paul Prabhakar Abhilash
Department of Accident and Emergency Medicine, Christian Medical College, Vellore  -  632  004, Tamil Nadu
India

Abstract

Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with Type 1 diabetes, but it is not uncommon in some patients with Type 2 diabetes. Fluid resuscitation, insulin administration, potassium administration, and correction of the underlying precipitating cause constitute the four pillars of treatment. Hyperglycemic hyperosmolar state (HHS) is classically seen in elderly patients with Type 2 diabetes. Although less common than diabetic ketoacidosis, HHS is associated with a higher mortality rate.



How to cite this article:
Abhilash KP. Hyperglycemic diabetic emergencies: Practice guidelines.Curr Med Issues 2017;15:208-210


How to cite this URL:
Abhilash KP. Hyperglycemic diabetic emergencies: Practice guidelines. Curr Med Issues [serial online] 2017 [cited 2023 Feb 3 ];15:208-210
Available from: https://www.cmijournal.org/text.asp?2017/15/3/208/212375


Full Text



 Introduction



Diabetes mellitus is a common metabolic disorder which may present to the emergency department with life-threatening emergencies. Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state/coma (HHS) are two common diabetic emergencies which can be managed with optimal fluid and blood glucose management along with optimization of electrolyte imbalances and treatment of the cause. This article discusses practical and concise guidelines for the diagnosis and management of these conditions that can be applied in almost any kind of hospital setting.

 Diabetic Ketoacidosis



DKA is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with Type 1 diabetes, but it is not uncommon in some patients with Type 2 diabetes. It may be the first manifestation of diabetes in many patients with Type 1 diabetes.[1],[2]

Clinical features

The most common early symptom of DKA is an insidious increase in polydipsia and polyuria.

Malaise, generalized weakness, fatigability, altered sensorium, and associated symptoms of infections may also be seen. Patients would be extremely dehydrated with a fluid deficit of at least 5–6 L.[2],[3]

Precipitating cause

Look for any precipitating cause and address itThe common precipitating causes (the five Is) are as follows:

Insulin – nonadherence to use of insulinInfection/inflammationIschemia/infarction (myocardial infarction/stroke)Intra-abdominal process – pancreatitis, cholecystitis, appendicitis, splenic injury, ischemic bowelIatrogenic – steroid use.

Diagnostic triad

The three features that form a triad that is diagnostic of DKA are:

High plasma sugar level (>250 mg%)Ketosis: Urine ketones positive (2+ or 3+. Remember that ketone 1+ positive is a common finding and does not mean ketosis)Acidosis: Serum bicarbonate <18 mEq/L or arterial blood gas (ABG) pH 

Key points:

Examination: If the glucometer random blood sugar is high, look for dryness of tongue and start intravenous fluids immediately before performing any testFluid resuscitation is lifesaving.

 Management



The four pillars of treatment are as follows:

Fluid resuscitationInsulin administrationPotassium administrationCorrecting the underlying precipitating cause.

Fluid resuscitation

This is the most important step. Start normal saline (NS) at the following rate (rule of diminishing by ½):

NS 1000 ml over 30 minNS 500 ml over 30 minNS 500 ml over 60 minNS 500 ml every 2 h till fluid deficit is corrected.

Tailor the above rates with the patient's cardiopulmonary status. Reassess every 2 h and look for fluid overload.

Insulin administration

Give a bolus of 10 units IV regular insulin (0.1 unit/kg) (to desaturate insulin receptor)Start insulin infusion at 0.1–0.2 units/kg/h and check the glucometer random blood sugar (GRBS) every 1 hThe excepted decline of the glucose per hour is 50–90 mg/dL. If not, increase the infusion by 2 units/h (consider a bolus of 4 units insulin if the GRBS is persistently high and does not show a decreasing trend)If significant hypokalemia exists (<3 mEq/L), do not start insulin infusion or give the bolus dose until IV KCl supplementation is initiated urgently. In smaller hospitals where ABG/venous blood gas facilities do not exist, insulin infusion can be commenced, but potassium supplementation should not be delayedWhen blood glucose levels reach 250 mg%, decrease insulin infusion to 4 units/h and change infusate to 5% dextrose. Do not stop insulin infusion. If blood sugars continue to drop, change infusate to 10% dextrose.[2],[3],[4]

Potassium correction

Metabolic acidosis and dehydration result in pseudo-hyperkalemia and the actual K levels may be lower than the result shownStart K + correction unless K+ level is >5 mEq/LIf K +Decrease the amount of KCl in patients with renal failure or if urine output is adequate.[5],[6]

Treat the precipitating cause

If there is any evidence of infection, start broad-spectrum antibiotics.

Correct severe metabolic acidosis

Administer NaHCO3 only if the serum pH <6.9. Give 100 ml bolus followed by 10 ml/h infusion.[5],[6]

Correct other electrolyte abnormalities:

Serum phosphate usually falls during treatment as it moves intracellularly with potassium.

Note:

Every patient with DKA should have at least three IV lines - one each for IV fluids, insulin infusion, and K correction. Additional lines for antibiotics or NaHCO3 may be needed. Start a central line at the earliest, if possible.

When to start oral feeds?

Oral feeds should be started when patient is conscious and alert, acidosis has improved (HCO3 >15 Meq/L), and when ketosis has resolved.

 Complications of Diabetic Ketoacidosis



Cerebral edema: It is mainly iatrogenic due to overcorrection of fluids. Headache, irritability, bradycardia, rising blood pressure, reducing conscious level, abnormal pupillary reflexes, cranial nerve palsies, and papilledema should arouse suspicionHypoglycemia and hypokalemia: This should be avoided by careful monitoring and adjustment of infusion rates. Increase glucose concentration of IV fluids, if serum glucose levels start falling quicklySystemic infection: Antibiotics are not given as a routine unless a severe bacterial infection is suspected (unusual infection, e.g., tuberculosis, fungal infections, and mucormycosis should be suspected in certain situations).Venous thrombosis (including central venous thrombosis): There is a significant risk of venous thrombosis in young and very sick children with DKA who have (a) central/femoral lines inserted (b) hyperosmolar state. Prophylactic anticoagulation with 100 units/kg/day of single daily dose of dalteparin (Fragmin) should be considered.Aspiration pneumonia: This can be avoided by inserting a nasogastric tube in patient with impaired consciousness and keeping the patient NPOAbdominal pain: It is common in DKA due to gastritis, bladder retention, or ileus. However, consider the possibility of appendicitis if the patient has right iliac fossa tenderness. A raised amylase level is common in DKA.

 Prevention of Recurrent Episodes



Parent/patient education, awareness creation on all aspects of DKA, is an essential part of any DKA management. Irregular/skipped insulin therapy, recent surgery, psychosocial stress, concomitant infection, and eating/behavioral disorders are the common precipitating causes for DKA. Prompt identification of infection and treatment with broad-spectrum antibiotics prevents recurrence.

 Hyperglycemic Hyperosmolar State



This condition is classically seen in elderly patients with Type 2 diabetes, although it may be seen in younger patients also.[7] Although less common than DKA, the mortality rate is higher in HHS.[7],[8] It is seen in the elderly who are bedbound with decreased thirst perception. Dehydration builds up slowly over time and hence is much worse than DKA. The usual predisposing factor is an infection [8]. This condition is characterized by hyperglycemia, dehydration, and serum hyperosmolarity without ketosis or significant acidosis.

Diagnosis

Diagnose HHS if the following are encountered:

Very high plasma glucose levelsHigh plasma osmolality: >350 mOsm/kgNo metabolic acidosis.

Differences between diabetic ketoacidosis and hyperglycemic hyperosmolar state

The amount of fluid deficit is much higher in HHS (average: 10–12 L)No ketosis or mild (urine ketone 1+) in HHSNo acidosis unless complicated by other conditions such as renal failure and sepsisGlucose levels are usually very high in HHSHypernatremia is common in HHS. If present, use ½ NS or ¼ NS as the replacement fluidUse lesser doses of insulin (typically half the dose used in DKA) in HHS as these patients may be more sensitive to insulin action.

Management

The management is similar to DKA management, except for the mentioned differences discussed above. Restrict fluids in those with congestive cardiac failure or pulmonary edema.

The type of fluid to be used is as follows:

Initial replacement: NSIf serum Na+ >155 mEq/L, use ½ NSOnce GRBS <250 mg%, change the infusate to 5% dextrose. Do not stop insulin infusion.

 Sliding Scale for Insulin Administration



[Table 1] summarizes the infusion rate according to the GRBS level (sliding scale). IV infusion of short-acting Actrapid insulin 1 ml (40 units) in 39 ml of NS (1 ml = 1 unit of insulin) has to be adjusted according to GRBS every 2 h (to be modified based on glycemic response).{Table 1}

Recovery and further management

Once recovered, the reason for the occurrence of HHS has to be addressed. Usually, during follow-up, most of the patients are likely to respond to oral antidiabetic drugs. Those at high risk should be monitored closely.

Financial support and sponsorship

Nil.

Conflicts of interets

There are no conflicts of interest.

References

1Faich GA, Fishbein HA, Ellis SE. The epidemiology of diabetic acidosis: A population-based study. Am J Epidemiol 1983;117:551-8.
2Newton CA, Raskin P. Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: Clinical and biochemical differences. Arch Intern Med 2004;164:1925-31.
3Dhatariya KK, Vellanki P. Treatment of diabetic ketoacidosis (DKA)/Hyperglycemic hyperosmolar state (HHS): Novel advances in the management of hyperglycemic crises (UK versus USA). Curr Diab Rep 2017;17:33.
4Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24:131-53.
5Magee MF, Bhatt BA. Management of decompensated diabetes. diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Crit Care Clin 2001;17:75-106.
6Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: A historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care 2014;37:3124-31.
7Cardoso L, Vicente N, Rodrigues D, Gomes L, Carrilho F. Controversies in the management of hyperglycaemic emergencies in adults with diabetes. Metabolism 2017;68:43-54.
8Frank LA, Solomon A. Hyperglycaemic hyperosmolar state. Br J Hosp Med (Lond) 2016;77:C130-3.