Endocrine Pathophysiology; Diabetes KetoAcidosis

The essay is based on a case study of a 21-year-old female A.M who presented to the urgent care clinic with nausea, vomiting, diarrhea, fever for 3days. She has type 1 diabetes and has not been managing her blood sugars since she’s been ill and unable to keep food down. She has been noncompliant with insulin medication since she is unable to eat and only tolerates sips of water and juices. She reports that her glucometer readings were high, vomits every time she takes fluid, has not voided for a day but voided the day before and she has been sleeping for longer hours and finally woke up this morning and decided to seek medical attention. On inspection, it is noted that she is unsteady, warm, and flushy skin and drowsy.her breathing is rapid and smells a fruity/sweet odor. She also has challenges in answering questions but asks for water to drink repeatedly.

Her current laboratory and vital signs are as follows:

Blood pressure88/46mmHg
Heart rate132beats per minute
Respiratory rate36breaths per minute
Temperature101.3 F( tympanic) 38.5 degree celsious
Glucose657mg/dl( 36.5 mmol/L)


The  above condition is caused by  deficiency in insulin thereby leading to hyperglycemia( blood glucose >11mmol/L or 200mg/Dl), metabolic acidosis( venous bicarbonate <15mmol/L and /or venous Ph <7.3) and hyperketonaemia( >3mmol/L) and ketonuria( >2+ on standard urine sticks) (Walker et all, 2018).

Insulin and glucagon are two important hormones that maintain blood sugar levels. They are counter-regulatory hormones. Insulin is produced by the beta cells in the pancreas. The presence of high blood glucose in the body leads to the production of insulin so that the peripheral tissues can utilize glucose. Absolute deficiency of insulin is interpreted as hypoglycemia by the pancreas. To counter this effect, glucagon is produced alongside cortisol, growth hormone, and epinephrine. Glucagon is produced by the alpha cells in the pancreas. This leads to a decrease in glucose utilization, increased proteolysis, increased lipolysis, increased glycogenolysis, and increased gluconeogenesis.

This in turn will lead to hyperglycemia ( decreased glucose utilization), hyperketonemia( increased production of ketone bodies ; acetoacetic acid, beta-hydroxybutyric acid, and acetone and decreased utilization of ketones bodies). When the accumulated ketones are unable to be extracted from the body, they are excreted through urine hence ketonuria.

            Etiology and clinical manifestation

The etiology of diabetes is caused by the destruction of beta cells of the pancreas causing deficiency of insulin. Diabetes ketoacidosis occurs as a complication of type 1 Diabetes mellitus.  The condition is precipitated by new-onset diabetes, non-adherence to insulin medication, poor control of the sugars, bacterial infections most commonly respiratory and intercurrent illnesses such as urinary tract infections, myocardial infarction, and surgical and emotional stress. Other factors include pancreatitis and endocrine pathologies such as acromegaly and intoxication.

 The above patient reported being non-compliant to her insulin medication. In this case, this would have been the main precipitating factor.  She reports having thirst, polydipsia, and polyuria. Hyperglycemia causes osmotic diuresis, therefore, leading to dehydration and electrolyte loss. Nausea, vomiting, and diarrhea would also lead to dehydration and electrolyte loss. Her skin is warm and flushy. Other signs of dehydration include cold extremities, dry mucosal membranes, and loss of skin turgor. From her vital signs, it noted that she had deep, labored rapid breathing known as Kussmaul breathing which is hyperventilation in response to metabolic acidosis. It was noted that she had a fruity odor that is due to the acetone produced as a ketone body. Her heart rate and respiratory rate were markedly elevated (tachycardia and tachypnea).  She has a reduced level of consciousness, as she appears drowsy and unsteady.  The potassium level is increased, 6.2mEq/L from the normal range of 3.5-5.5mEq/L. Some of the constitutional symptoms present are fever of 38.5 degrees Celsius which indicates an infection. Others include cough, chills, chest pains, and arthralgia.

            Laboratory investigations

Blood glucose7.0-11.0 mmol/LTo measure the glucose level in blood. Hyperglycemia is a diagnostic criterion of diabetes ketoacidosis.
Venous blood gas7.00-7.30To elicit metabolic acidosis.
HBA1c7%For glycemic control
Serum ketonesBeta-hydroxybutyric acid > 3.8mmol/LDiagnostic criteria
UrinalysisPositive for glucose and ketones 
Serum potassium 3.5-5.5 mmol/LElevated due to the extracellular shift caused by insulin deficiency.

 Other investigations includeLipid profile, complete blood count, liver function tests, urea, electrolytes and creatinine, thyroid function test, bicarbonate levels, serum lactate, stool for over, and cyst.  The imaging modalities that would be helpful include; chest X-ray and electrocardiogram.


The patient needs to be admitted to the ward and the stabilized: Airway, Breathing, Circulation, Dysfunction. Then diagnosis is made by taking a clear history and investigations. This is followed by correcting the dehydration using intravenous fluids i.e start with  0.9% normal saline: 1L for the first 1hour, 1L for the next 2nd hour, 1L for over the next 2hours, and then 1L every 4hours, then switch to 5% dextrose 1L 8hourly. Thereafter insulin therapy should be started about half an hour after the initiation of fluids while monitoring potassium levels. It is given at a rate of 0.1U/kg/hour using an infusion pump. Then manage potassium levels by administering potassium chloride. Blood glucose, potassium level, urine output should be monitored. A prophylactic antibiotic is administered.

Reference list.

Muneer, M., & Akbar, I. (2020). Acute Metabolic Emergencies in Diabetes: DKA, HHS, and EDKA.

Ralston, S. H., Penman, I. D., Strachan, M. W., & Hobson, R. (Eds.). (2018). Davidson’s Principles and Practice of Medicine E-Book. Elsevier Health Sciences.

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