Case 1: Jane is a twelve-year-old female who has begun to have a variety of problems at school. She has been losing weight and is concerned because she has not yet achieved menarche, unlike many of her friends. Her schoolwork has begun to suffer. She is fatigued and has trouble concentrating; she has difficulty participating in athletics, and her vision is occasionally blurred. She is embarrassed because her teacher has noticed that she frequently must ask to go to the rest room and is constantly drinking. While trying to exercise in the gym, she faints and is taken to the hospital by ambulance. Her temperature is normal. Respirations are rapid and deep. Blood pressure is normal. She is comatose but responded to painful stimuli. Her skin is warm and dry. The remainder of the physical signs are normal. The patient’s urine contained large amounts of glucose. There was a strongly positive reaction for acetone and other ketone bodies. Blood glucose was 565 mg/dl (normal range 60–100 mg/dl). Other laboratory studies revealed a low blood pH and reduced plasma bicarbonate of 8 mEq/l (normal range 24–28 mEq/l). The patient was considered to have severe diabetic acidosis probably precipitated by stress during exercise. After intensive treatment with intravenous fluids and insulin, her condition gradually improved. The following day she was conscious and oriented and was able to take fluids orally. She continued to improve and was eventually discharged from the hospital. Testing revealed a moderately elevated level of hemoglobin A1c. She was diagnosed with type 1 diabetes mellitus and instructed in the details of a diabetic diet and taught to do frequent self-monitoring for blood glucose levels. She required a minimum of two injections of insulin with occasional supplementation with a rapid-acting inhaled insulin prior to strenuous exercise. She is now doing well in school and is monitored regularly by a physician specializing in diabetes in the young.
Case 2: John is an obese, sixty-eight-year-old man who was diagnosed several years ago as being prediabetic on the basis of a borderline abnormal glucose tolerance test and minimally elevated hemoglobin A1c. He was also been found to be moderately hypertensive at that time, but John has not seen a physician since nor has he modified his sedentary lifestyle. He has experienced increased urinary output and thirst for the last two weeks. He attends the North Carolina State Fair on an extremely warm and humid day and consumes large quantities of sugar-containing soft drinks, cotton candy, and fried chocolate candy bars. He becomes progressively more confused and collapses in a coma. He is brought to the hospital by the local emergency rescue squad with a suspicion of heat exhaustion, but his temperature is only slightly elevated. On admission, he is comatose and dehydrated. His respiratory rate is not increased. Blood pressure is normal. The urine contains a large amount of glucose but no ketone bodies. Blood pH and bicarbonate are normal. Blood glucose is 1,750 mg/dl (normal range 60–100 mg/dl), and the osmolarity of the plasma is 396 mOsm/ liter (normal range 280–295 mOsm/liter). A diagnosis of hyperosmolar nonketotic coma is made. He is treated with large volumes of hypotonic (0.45 percent) saline solution and with insulin. His condition gradually improves over the next several days. His blood glucose gradually falls toward normal and eventually reaches 150 mg/dl on the fourth day. Plasma osmolarity also returns to normal as the elevated blood glucose declines. He is diagnosed as having type 2 diabetes mellitus and is instructed to lose weight and begin a moderate exercise program. He is placed on an oral hypoglycemic agent (metformin) but also requires supplemental insulin to control his blood glucose level. He does forswear high-sugar snacks in future visits to the fair.
Discussion
The purpose of these cases is to illustrate some of the typical symptoms of type 1 and type 2 diabetes mellitus and acute medical problems associated with each. It is not uncommon for emergency medical responders to be required to diagnose and begin therapy for ketoacidosis, hyperosmolar coma, and insulin shock (the latter not illustrated in the cases). Table 22-2 summarizes the differential signs of each. Type 1 and type 2 diabetes mellitus are both characterized by hyperglycemia, but the etiologies and presentations of the diseases are quite different. Although acute complications of both diseases may differ, the chronic multisystem effects of poorly controlled disease are similar.
Table 22-2
Etiology and Pathogenesis
Case 1 is undiagnosed type 1 diabetes mellitus associated with autoimmune destruction of the pancreatic islets and consequent lack of sufficient insulin production. A common acute presentation (diabetic ketoacidosis) relates to the production of acidic metabolic products of excessive lipid metabolism, which exceed the buffering capacity of the plasma. Case 2 demonstrates the progression of prediabetes into symptomatic type 2 diabetes in an individual suffering from uncontrolled metabolic syndrome. In this case, increasing insulin resistance related to obesity and lifestyle progress to the point at which extreme hyperglycemia related to the sudden intake of massive amounts of sugar occurs.
Questions
1. Type 1 diabetes mellitus (unlike type 2 diabetes mellitus) is often discovered when a person suffers from the sudden occurrence of ketoacidosis. Why do the two diseases differ in this respect?
2. Type 1 and type 2 diabetes mellitus both result in hyperglycemia, but the etiologies are distinct. What are the likely etiologies for the two conditions?
3. How are the symptoms and clinical signs of both forms of diabetes related to the pathophysiology of the diseases?
4. The second case description states the patient has metabolic syndrome. What is this syndrome, and how does the description of the patient support this? What is the relationship of metabolic syndrome to type 2 diabetes mellitus?