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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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8
Endocrinology
Case 1
Chief Complaint
Lower abdominal pain, dysuria, weakness, and lethargy for 2 days.
History and Physical Examination
A 17-year-old girl comes to the emergency department with lower abdominal pain,
increasing weakness, and lethargy for 2 days. Her family has noticed a decreased
appetite, nausea, and vomiting. For the last month they have also noticed that the patient
has been complaining of being thirsty, going to the bathroom to urinate constantly, and has
lost weight.
Her T is 37.8 C (100.0 F), BP 100/70 mm Hg, pulse 130/min, and respirations 32/min.
She is ill appearing and lethargic. She answers questions with difficulty but appropriately.
Physical examination shows a fruity odor on her breath, dry oral mucosa, a supple neck,
no jugular venous distension, equally round and reactive pupils, and clear lungs. The heart
has a regular rhythm and is tachycardic. The suprapubic abdomen is tender to deep
palpation. Neurologic examination shows no obvious focal deficits.
411
CLINICAL PEARL
Breath that has a fruity odor is caused by acetone and suggests ketoacidosis.
Differential Diagnosis
Diabetic ketoacidosis (DKA)
1.
Patient has signs and symptoms of diabetes mellitus (DM) including polydipsia,
polyuria, and weight loss. DKA is often the initial presentation of type 1 DM in a
young adult. It can present with intravascular volume depletion and altered mental
status.
—
Meningoencephalitis
2.
Presents with altered mental status and fever; most common causes in United States
are herpes simplex virus and West Nile virus; the presence of polyuria, polydipsia
and weight loss in preceding month argue against this diagnosis
—
Sepsis secondary to UTI
3.
Can present with fever and altered mental status, but almost exclusively in elderly
patients.
—
Abdominal infection
4.
Appendicitis can present with fever, nausea, vomiting and abdominal pain. Again,
the presence of other symptoms for the past 1 month make this acute diagnosis less
likely.
—
Drug overdose
5.
Usually does not present with fever, however should always be ruled out in young
—
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Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
CCS NOTE
The Step 3 exam requires you to learn diagnostic tests and treatment plans, as well as
the order in which they are performed. In a tachycardic patient with nausea and
vomiting, IV fluids should always be included in the initial set of orders.
Test Results
adults presenting with altered mental status.
Plasma glucose, serum electrolytes, serum creatinine and BUN; CBC with differential
Urine studies: urinalysis, urine culture, urine ketones, beta hCG
Arterial blood gas
EKG
CT abdomen/pelvis
Lumbar puncture
Toxicology screen
Monitor vital signs; start O
2
via nasal cannula; start IV hydration with normal saline +/- IV
antibiotics
Biochemical profile: Sodium 130 mEq/L (normal: 135–145 mEq/L), potassium 5.5 mEq/L
(normal: 3.5–5.2 mEq/L), chloride 100 mEq/L (normal: 96–108 mEq/L), bicarbonate 7.5
413
Assessment
The history suggests that the patient has new onset diabetes. She has polyuria, polydipsia, and
weight loss for 1 month. The patient now presents to the emergency department because the
disease has suddenly progressed to acute illness with abdominal pain and altered mental status.
Labs show a severe anion gap metabolic acidosis with urinary ketones, supporting a diagnosis
of ketoacidosis. The patient also has hyperglycemia and glucosuria, supporting a diagnosis of
diabetes, likely type 1. As a result of the hyperosmolar diuresis and nausea/vomiting, the
patient also has intravascular volume depletion, which induced acute kidney injury.
CCS NOTE
Severe metabolic acidosis with a very low serum bicarbonate is an indication for
placing the patient into the ICU.
Given these findings along with a negative lumbar puncture, CT abdomen and pelvis, and
toxicology screen, the other diagnoses on the differential become less likely. The patient is in
mEq/L (normal: 20–24 mEq/L), BUN/creatinine 65 mg/dL / 2.5 mg/dL (normal: 10–20
mg/dL / 0.6–1.2 mg/dL), glucose 490 mg/dL (normal: 80–120 mg/dL)
CBC: WBC 15.9 with 90% neutrophils on differential
Urinalysis: WBCs 60, +leukocyte esterase, +glucose, +ketones; beta hCG negative; urine
culture pending
Arterial blood gas: pH 7.26, pCO
2
16, pO
2
128, HCO
3
- 7.5
EKG: sinus tachycardia
CT abdomen/pelvis: negative
Lumbar puncture: 0 WBC, normal glucose and protein
Toxicology screen: negative
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diabetic ketoacidosis, a life-threatening condition.
A common precipitant of diabetic ketoacidosis is an infection, which increases the body’s
insulin requirement. In this case, the patient’s UTI was likely the cause. Symptoms of severe
diabetic ketoacidosis include altered mental status which can progress to coma, as well as
nausea, vomiting, abdominal pain, and hyperventilation.
The differential diagnosis for altered mental status is broad, and includes metabolic, infectious,
toxic, endocrine, and neurologic causes. A careful history and physical exam can aid in
narrowing down which tests are initially ordered in the work up.
CLINICAL PEARL
A mnemonic to recall the differential diagnosis of altered mental status without focal
neurological deficits in decreasing order of frequency is DIM:
Basic Science Correlate
Diabetic ketoacidosis is primarily a complication of type 1 DM. It can result from
omission of insulin or medical illness. The condition can develop in a matter of hours
if a patient has complete insulin deficiency. Because it occurs rapidly, glucose levels
are typically lower than those seen in hyperosmolar nonketotic coma, which occurs in
Drugs (adverse effects or overdose)
Infections
Metabolic (sodium, glucose, calcium, renal)
415
uncontrolled type 2 DM and may be subacute in presentation. Insulin normally inhibits
hormone-sensitive lipase. Uninhibited, hormone-sensitive lipase releases fatty acids,
which are then converted to acetyl CoA, which is converted to ketone bodies in the
liver. Even a small amount of endogenous insulin can prevent this process. This is why
diabetic ketoacidosis is rarely a complication of type 2 DM. Patients with type 2 DM
usually have some degree of endogenous insulin production.
CCS NOTE
With severe hyperglycemia, the osmolality of the extracellular fluid rises and water
shifts to the extracellular space, causing a decrease in the sodium concentration. Serum
sodium decreases by 1.6 mEq/L for every 100 mg/dL of glucose above normal. There
is no net change in total body water, and when the glucose is corrected, the sodium
concentration will return to normal.
The primary mechanism for hyperglycemia is increased hepatic gluconeogenesis.
Glucagon and epinephrine are the hormonal signals that increase gluconeogenesis. In
an insulin-deficient state, glucagon and epinephrine are increased. There is also
some degree of glycogenolysis from the liver, but this is short lived.
Acidosis and electrolyte abnormalities can be life-threatening by inducing cardiac
arrhythmias. Total body potassium is usually low, though initially the serum
potassium may appear normal to high because of the metabolic acidosis
(transcellular shift of K+ out of cell for H+ into cell). Phosphorus and magnesium
may also be depleted.
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Further Management
CLINICAL PEARL
Insulin will move glucose and phosphate into the cell simultaneously. Additionally, as
the acidosis improves, serum K
+
will decrease. Severe hypokalemia or
hypophosphatemia can cause respiratory paralysis. Monitor and replace these
electrolytes aggressively.
Discussion
Type 1 DM compromises 5% of all diabetes. It is caused by autoimmune destruction of the
insulin secreting pancreatic beta cells, possibly triggered by a viral infection. Additionally,
HLA susceptibility genes found in regions on chromosome 6 may play a role. It usually
presents with DKA. The patient may have an antecedent history of fatigue, polyuria,
Admit patient to ICU
Use aggressive fluid resuscitation with cystalloids (0.9% normal saline); change fluids to
D5 1/2NS once glucose level falls to <250 mg/dL
Give bolus of regular insulin, then start insulin drip; continue this until anion gap is closed,
then give dose of subcutaneous insulin before stopping the drip; continue treatment with
subcutaneous insulin
Monitor glucose and electrolytes (K
+
, Mg
2+
, PO
4-
) every 2–4 hours and replete as needed;
add K
+
to fluids to keep up with replacement
Check blood cultures
Check blood for ketones
Check hemoglobin A1c (so there is a baseline)
Start antibiotics for UTI
417
polydipsia, polyphagia, dehydration and blurry vision. In DKA, patients will experience
nausea, vomiting, abdominal pain and altered mental status. DKA can be precipitated by an
acute infection or severe stress.
DKA is a life-threatening complication of type 1 DM and it is usually managed in an ICU
setting. Management involves aggressive fluid resuscitation, replacement of insulin and
electrolytes, and treatment of any underlying infection.
CCS NOTE
When there is evidence of infection (e.g., fever) and WBC in the urine, always begin
antibiotics before obtaining the results of the urine culture.
Follow-up Management and Prevention
Long-term treatment for type 1 DM is insulin. This usually consists of long-acting basal insulin
administered 1× a day, and ultra-short-acting insulin given prior to meals. Alternatively, a
subcutaneous insulin pump may be used for continuous infusion, with the ability to bolus for
meals or during increased periods of stress.
These regimens allow for more precise control of blood glucose and avoidance of
hypoglycemia. Fasting and pre meal target glucose is 80–130 mg/dL. Post prandial levels
should not exceed 180 mg/dL. Goal HgA
1
C is <7% in nonpregnant adults with a long-life
expectancy, and should be monitored at 3–6 month intervals.
Of note, the “honeymoon” period (in insulin-dependent DM patients) is an initial episode of
ketoacidosis followed by a symptom-free interval. Although the patient’s insulin requirement
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during this phase may be minimal, a small amount of insulin should be continued as the disease
will progress.
Final Diagnosis
Diabetic ketoacidosis
419
Case 2
Chief Complaint
Confusion
History and Physical Examination
A 49-year-old obese man is brought to the emergency department by his wife because he
is “not himself.” He was very drowsy and not eating much for the last 4 days. He was
making urine every hour and was drinking water because he felt thirsty. His wife had not
noticed any fever, chills, nausea, or vomiting. He was known to be hypertensive for 10
years and takes hydrochlorothiazide. About 2 years ago he was told by his doctor that he
had borderline diabetes mellitus and was started on a diet. No medications were
prescribed at that time.
On examination today his T is 37.7 C (99.9 F), BP 100/60 mm Hg, pulse 110/min with
orthostasis, and respirations 20/min. SpO
2
is 98% on room air. He appears very lethargic.
He is arousable but responds incoherently to questions. He orients only to his name, and
has no idea where he is or who his wife is. Lung examination is normal with good air
entry. Heart exam shows tachycardia, but a normal rhythm without a murmur. There are no
focal neurologic signs, and the rest of the physical examination is unremarkable.
Differential Diagnosis
Hyperosmolar hyperglycemic nonketotic syndrome (HHNS)
1.
A complication of type 2 DM; presents with altered mental status and intravascular
—
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