Case Histories Flashcards
A 12-year-old white girl is brought to the emergency department by her parents due to 12 hours of rapidly worsening nausea, vomiting, abdominal pain, and lethargy. Over the last week she has felt excessively thirsty and has been urinating a lot. Physical examination reveals a lean, dehydrated girl with deep rapid respirations, tachycardia, and no response to verbal commands.
Type 1 diabetes mellitus
Type 1 diabetes presents with polyuria, polydipsia, weight loss, generalised weakness, and blurred vision. Some patients present with diabetic ketoacidosis, the acute complication of type 1 diabetes. These patients have symptoms of dehydration and acidosis such as nausea, vomiting, abdominal pain, tachypnoea, tachycardia, and lethargy. Rarely, a patient is diagnosed with type 1 diabetes during routine blood tests. The condition is diagnosed long before its chronic complications have developed
The rate of beta-cell destruction varies in type 1 diabetes. In some patients, there may be a slow destruction leading to gradual onset of symptoms that is clinically indistinguishable from type 2 diabetes. When the initial presentation of type 1 diabetes occurs in adulthood, some refer to it as latent autoimmune diabetes in adults (LADA). It is useful to distinguish LADA from type 2 diabetes, because patients with LADA usually require insulin therapy. Features that suggest the presence of LADA rather than type 2 diabetes include 2 or more of the following: age of onset less than 50 years, acute symptoms, BMI less than 25 kg/m^2, and personal or family history of autoimmune disease.
An overweight 55-year-old woman presents for preventative care. She notes that her mother died of diabetes, but reports no polyuria, polydipsia, or weight loss. BP is 144/92 mmHg, fasting blood sugar 8.2 mmol/L (148 mg/dL) (on 2 occasions), HbA1c 65 mmol/mol (8.1%), LDL-cholesterol 5.18 mmol/L (200 mg/dL), HDL-cholesterol 0.8 mmol/L (30 mg/dL), and triglycerides 6.53 mmol/L (252 mg/dL).
Type 2 DM
Type 2 diabetes is most often diagnosed on routine screening. Strong risk factors, which also indicate the need for screening, include: older age; overweight/obesity; black, Hispanic, or Native American ancestry; family history of type 2 diabetes; history of gestational diabetes; presence of pre-diabetes; physical inactivity; polycystic ovary syndrome; hypertension; dyslipidaemia; or known cardiovascular disease. [2] Symptomatic patients may present with: fatigue; polyuria, polydipsia, polyphagia, or weight loss (usually when hyperglycaemia is more severe [e.g., >16.6 mmol/L, >300 mg/dL]); blurred vision; paraesthesias; unintentional weight loss; nocturia; skin infections (bacterial or candidal); urinary infections; or acanthosis nigricans.
Other presentations:
Patients with type 2 diabetes can also present with symptoms such as blurred vision; fatigue; erectile dysfunction; urinary tract or candidal infections; dry itchy skin; paresthaesias; increased urination, thirst, and appetite; or unexplained weight loss
A 20-year-old man is brought to the accident and emergency department with abdominal pain, nausea, and vomiting with increasing polyuria, polydipsia, and drowsiness since the previous day. He was diagnosed with type 1 diabetes 2 years previously. He mentions that he ran out of insulin 2 days ago. Vital signs at admission are: BP 106/67 mmHg, heart rate 123 beats per minute, respiratory rate 32 breaths per minute, temperature 37.1°C (98.8°F). On mental status examination, he is drowsy. Physical examination reveals Kussmaul breathing with acetone odour and mild generalised abdominal tenderness without guarding and rebound tenderness. Initial laboratory data are: blood glucose 25.0 mmol/L (450 mg/dL), arterial pH 7.24, pCO2 25 mmHg, bicarbonate 12 mmol/L (12 mEq/L), WBC count 18.5 × 10^9/L (18,500/microlitre), sodium 128 mmol/L (128 mEq/L), potassium 5.2 mmol/L (5.2 mEq/L), chloride 97 mmol/L (97 mEq/L), serum urea 11.4 mmol/L (32 mg/dL), creatinine 150.3 micromol/L (1.7 mg/dL), serum ketones strongly positive.
Diabetic ketoacidosis:
Kussmaul breathing = (deep and rapid respiration due to ketoacidosis)
It is now well recognised that new-onset type 2 diabetes can manifest with DKA. These patients are obese and have undiagnosed hyperglycaemia, impaired insulin secretion, and insulin resistance. However, after treatment of the acute hyperglycaemic episode with insulin, beta-cell function and insulin effects improve, so these patients are able to discontinue insulin therapy and may be treated orally or by diet alone, with 40% remaining insulin-independent 10 years after the initial episodes of DKA. These patients do not have the typical autoimmune laboratory findings of type 1 diabetes. [2] This type of diabetes has been labelled as ‘type 1 and 1/2’ or ‘type 1 and a half’ diabetes, ‘Flatbush’ diabetes, or ‘ketosis-prone’ diabetes. Conversely, an extreme hyperosmolar state similar to hyperosmolar hyperglycaemic state (HHS) has been reported in combination with DKA in type 1 diabetes. [3] [4] [5] [6]
A 72-year-old man is brought to hospital from a nursing home for progressive lethargy. The patient has a history of hypertension complicated by a stroke 3 years previously. This has impaired his speech and rendered him wheelchair-bound. He also has a schizothymic disorder for which he was started recently on clozapine. On presentation, he is disoriented to time and place and febrile, with a temperature of 38.3°C (101°F). Vital signs include a BP of 106/67 mmHg, heart rate of 106 beats per minute, and a respiratory rate of 32 breaths per minute. Initial laboratory work-up reveals a serum glucose of 52.7 mmol/L (950 mg/dL), a serum sodium of 127 mmol/L (127 mEq/L), a serum urea of 21.1 mmol/L (59 mg/dL), and a serum creatinine of 175.4 micromol/L (2.3 mg/dL). Serum osmolality is calculated as 338 mmol/kg (338 mOsm/kg). Urinalysis reveals numerous white blood cells and bacteria. Urine is positive for nitrates but negative for ketones. Serum is negative for beta-hydroxybutyrate.
Hyperosmolar hyperglycaemic state
Hyperosmolar hyperglycaemic state (HHS), also known as non-ketotic hyperglycaemic hyperosmolar syndrome (NKHS), is characterised by profound hyperglycaemia (glucose >33.3 mmol/L [>600 mg/dL]), hyperosmolality (effective serum osmolality ≥320 mmol/kg [≥320 mOsm/kg]), and volume depletion in the absence of significant ketoacidosis (pH >7.3 and HCO3 >15 mmol/L [>15 mEq/L]), and is a serious complication of diabetes. HHS may be the first presentation of type 2 diabetes.
HHS Occurs most commonly in older people with type 2 diabetes. Contributes to less than 1% of all diabetes-related admissions. However, mortality is high (5% to 15%).
Although both HHS and diabetic ketoacidosis (DKA) are often discussed as distinct entities, they represent 2 points on the spectrum of metabolic derangements in diabetes. [3] Both HHS and DKA are characterised by relative or absolute insulin deficiency combined with increased counter-regulatory hormones. [1] [4] Approximately 33% of patients with hyperglycaemic crises present with a mixed picture of DKA and HHS
A 45-year-old man with a history of type 2 diabetes is admitted directly from clinic for a serum glucose of 53.8 mmol/L (970 mg/dL). He was started recently on basal bolus insulin therapy after several years of treatment with oral antiglycaemic agents. However, he reports not having followed his insulin prescription owing to its high cost. For the past 2 weeks he has had polyuria and polydipsia, and has lost 5 kg in weight. He has also noted a progressively worsening cough for approximately 3 weeks that is productive of greenish-brown sputum. On examination, he is febrile, with a temperature of 38.5°C (101.3°F), tachypnoeic (respiratory rate of 24 breaths per minute), and normotensive. Urinalysis reveals trace ketones, but serum beta-hydroxybutyrate is not elevated. Serum bicarbonate is 17 mmol/L (17 mEq/L), and venous pH is 7.32
Hyperosmolar hyperglycaemic state
Up to 20% of patients admitted with hyperosmolar hyperglycaemic state (HHS) have previously undiagnosed diabetes. [1] [5] [6] [7] Approximately 33% of patients with hyperglycaemic crises present with a mixed picture of diabetic ketoacidosis and HHS. [5] Coma is a rare presentation of HHS. Typically, coma is associated with serum osmolality levels >330 to 340 mmol/kg (>330-340 mOsm/kg) and is most often due to hypernatraemia rather than hyperglycaemia. Occasionally, patients with HHS may present with seizures or hemiparesis. [8] A mild acidaemia and ketoacidosis may often be present.
