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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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CCS NOTE
The least crucial part of the CCS is the Final Diagnosis. A correct clinical process is
preferred over a correct but rushed diagnosis. You will never lose points for getting a
sodium, glucose, or calcium level in a delirious patient.
Initial Management Plan
Setting: emergency department
volume depletion; plasma osmolality is typically >320 mosm/kg and plasma glucose
>600 mg/dL in the absence of serum ketones and metabolic acidosis
Other metabolic etiologies: electrolyte disorders: hypercalcemia and
hyper/hyponatremia
2.
In particular, severe hypercalcemia also presents with altered mental status and
profound volume depletion; other diagnoses include hypoxia/hypercapnea,
hyper/hypo thyroidism, hepatic encephalopathy, uremic encephalopathy, and drug
intoxication or withdrawal.
—
Infections: sepsis secondary to a UTI, pneumonia and encephalitis/meningitis3.
Oftentimes, an infection alone can present with altered mental status but infection
can also precipitate HHNS; an infectious work up should always be pursued
—
Stroke4.
Less likely given altered mental status without other focal abnormalities—
Structural lesion: brain tumor or abscess5.
421
Diagnostic/Therapeutic Plan
Test Results
Assessment
Both diabetic ketoacidosis (DKA) and HHNS are complications of DM, typically type 1 DM
and type 2 DM, respectively. Both DKA and HHNS may be associated with altered mental
status and dehydration. Patients with DKA have ketones in the serum and urine, an anion gap
metabolic acidosis, and a blood pH <7.3. In HHNS, serum and urine ketones are absent, there
Electrolytes, glucose, BUN, creatinine, serum osmolality, LFTs, thyroid function tests,
ammonia level
CBC with differential
Urinalysis
Lumbar puncture
Chest x-ray
CT head without contrast
Urine drug screen
Sodium 130 mEq/L, potassium 5.2 mEq/L, chloride 95 mEq/L, bicarbonate 24 mEq/L,
BUN/creatinine 58 mg/dL/2.2 mg/dL, glucose 998 mg/dL, serum osmolality 336 mOsm/kg,
calcium 9.8 mg/dL, total protein 7.3 g/dL, albumin 4.2 g/dL, AST 13 u/mL, ALT 20 u/mL,
total bilirubin 0.3 mg/dL, alkaline phosphatase 71 u/mL, TSH 0.86 mlu/mL, ammonia 30
mcg/dL
WBC 15,000/mm
3
, hemoglobin 15.5 gm/dL, platelets 354 k/uL; unremarkable differential
Urinalysis: specific gravity 1.029, 4
+
glucose, 2
+
protein, no WBCs
Lumbar puncture normal
Chest x-ray normal
CT head non-contrast normal
Urine drug screen negative
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may be a mild metabolic acidosis (usually none at all), and blood pH is >7.3. Additionally,
patients with HHNS have very high blood sugars, often above 600 mg/dL which cause an
osmotic diuresis inducing severe intravascular volume depletion.
The patient’s lab results support the diagnosis of HHNS. His antecedent history of borderline
DM is the key historical clue. He has acute kidney injury, likely pre-renal in origin from
extremely high glucose levels. In turn, the high serum glucose has elevated his serum
osmolality, and is the driver of both the intravascular volume depletion and altered mental
status.
The other diagnoses on the differential are effectively ruled out given normal LFTs, calcium,
TSH, ammonia, lumbar puncture, CXR, and CT head. Patient does have low serum sodium, but
this is falsely low because of hyperglycemia.
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. The
serum sodium level decreases by 1.6 mEq/L for every 100 mg/dL of glucose above
normal.
Basic Science Correlate
Pre-renal azotemia is characterized by an increase in BUN and plasma creatinine due
to decreased blood flow to the kidneys. The decreased blood flow to the kidneys
causes increased renin secretion via RAS axis, which in turn increases aldosterone
423
secretion. Aldosterone causes reabsorption of sodium and wasting of potassium and
hydrogen ion. This mechanism aims to preserve sodium in order to stabilize the loss of
intravascular volume.
CLINICAL PEARL
Coronary artery disease may present in a typical fashion or may be silent in patient
with diabetes. ‘Silent ischemia’ has been associated to cardiac autonomic neuropathy.
New-onset uncontrolled hyperglycemia and hyperosmolar hyperglycemic state (with or
without the presence of dyspnea) may be a presentation of an acute coronary syndrome
in patients with diabetes.
Further Management Plan/Results
Initial fluid resuscitation in the emergency department with large volumes of normal
saline intravenously. Admission to general medical ward or ICU depending on patient’s
status after initial volume resuscitation. Fluid replacement is the cornerstone of HHNS
management.
1.
Insulin
2.
Monitor vital signs and labs closely, especially fingerstick, serum electrolytes, and
renal function. Replete lytes as needed. Often, potassium can be added to fluids as total
body potassium is low from the osmotic diuresis.
3.
Search for and treat the underlying cause of the HHNS. As is often the case with DKA,
HHNS usually has a precipitating factor (infection, infarction, intoxication, medical
noncompliance).
4.
Collect blood and urine cultures
5.
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Discussion
Type 2 DM is associated with obesity and insulin resistance. It has a strong genetic
predisposition. It accounts for approximately 90% of DM cases in the United States. Secondary
causes of type 2 DM include Cushing’s syndrome, exogenous steroid administration, other
medications (thiazides, phenytoin, pentamidine), cystic fibrosis, and chronic pancreatitis.
CCS NOTE
The case simulations do not ask for specific levels of fluids. You can specify either
bolus or continuous only. You can repeat the bolus and recheck vital signs.
HHNS is an acute complication of DM that occurs predominantly in patients with type 2 DM. It
is characterized by severe hyperglycemia in the absence of significant ketosis. Precipitating
factors include noncompliance with treatment, infection, infarction, and other stressors. The
pathogenesis is hyperglycemia causing an osmotic diuresis followed by the inability to drink
sufficient water to keep up with urinary losses. It is clinically manifested by weakness,
polyuria, polydipsia, lethargy, confusion, and coma. From an epidemiological standpoint, the
patient is usually an elderly type 2 diabetic.
The diagnosis of HHNS is suggested by profoundly elevated blood glucose (1,000 mg/dL) and
serum osmolality (serum osmolality in mOsmol/kg H
2
O = 2 [sodium] + BUN/2.8 + serum
glucose/18). Acute kidney injury may also be present if the patient is extremely volume-
depleted. Serum bicarbonate levels are usually normal (or a mild metabolic acidosis in some
cases) and blood pH is >7.3. Serum and urine ketones will be absent.
Check EKG6.
425
Chronic complications of DM involve both the micro- and macrovasculature. Retinopathy,
nephropathy and neuropathy are considered microvascular complications. Macrovascular
complications include increased risk of MI, stroke and peripheral vascular disease. Evidence
shows that lowering the hemoglobin A1c prevents microvascular complications, but may not
prevent macrovascular complications. The primary treatment for macrovascular complications
is risk factor control with BP and cholesterol lowering medications as well as prophylaxis
with anti-platelet agents.
Treatment for type 2 DM primarily involves oral hypoglycemic agents. Metformin is
considered first line therapy in all type 2 diabetics. Insulin is usually reserved for patients that
remain uncontrolled on multiple oral hypoglycemic agents.
Follow-up Management and Prevention
Diabetes is a chronic disease. It requires regular monitoring to prevent acute complications (as
in this case) as well as micro- and macrovascular complications. Goal hemoglobin A1c is
<7% and should be monitored every 3–6 mos. BP should be monitored at every office visit
(new JNC 8 guidelines suggest goal BP <140/90 mm Hg). Newer cholesterol guidelines
suggest all diabetic patients should be placed on a statin medication and lipid profile should be
monitored annually.
The diabetic patient also requires annual dilated eye exam and foot exam. Additionally, the
urine should be checked for the presence of microalbumin on an annual basis. An ACEI or
ARB should be initiated if microalbumin is detected in the urine.
Other important health care maintenance in the diabetic patient includes annual influenza
vaccine and a one time pneumococcal vaccine (repeat 1× if first dose given age <65 and >5 yrs
ago).
Final Diagnosis
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Hyperosmolar hyperglycemic nonketotic syndrome
427
Case 3
Chief Complaint
Increased serum calcium on routine medical evaluation
History and Physical Examination
A 30-year-old man comes to your office for the evaluation of hypercalcemia, noted on
routine tests performed at his workplace. He denies any specific complaints and is not
taking any medications. His past medical history is significant for several episodes of
renal stones 2 to 3 years ago. Physical examination is unremarkable.
Differential Diagnosis
Initial Management
Setting: outpatient
Diagnostic/Therapeutic Plan
Primary hyperparathyroidism
1.
Malignancy
2.
Sarcoidosis
3.
Familial hypocalciuric hypercalcemia
4.
Basic metabolic panel (sodium, potassium chloride, bicarbonate)
Serum calcium
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Test Results
Assessment
Most cases of asymptomatic hypercalcemia in young ambulatory patients are caused by primary
hyperparathyroidism. Given the history of renal stones 2 years ago, the patient probably has
had increased serum calcium for a long time without any other problems. The age of the patient
and the benign course of his hypercalcemia make a diagnosis of malignancy less likely, but
malignancy should always be ruled out in cases where History and Physical Examination
suggest it.
CCS NOTE
Asymptomatic patients should always remain out of the hospital. Such patients should
be sent home between office visits.
Malignant diseases can lead to hypercalcemia via parathyroid hormone-related proteins or by
bone metastases. Other causes of hypercalcemia include drugs (thiazides, lithium),
granulomatous diseases (sarcoidosis), thyrotoxicosis, and immobilization.
Chest x-ray
Urine calcium
Basic metabolic panel WNL
Serum calcium 11.3 mg/dL (normal: 8.5–10.3 mg/dL)
Chest x-ray normal
Urine calcium elevated
429
Familial hypocalciuric hypercalcemia is a benign condition that can be diagnosed by checking
urinary calcium levels (<200 mg/24 h) combined with a family history of similar conditions
and normal parathyroid hormone levels.
Further Diagnostic Plan/Results
Immunoassay for serum parathyroid hormone 22 mEq/mL (normal: 4–9 mEq/mL)
Treatment Plan
Discussion
The higher level of parathyroid hormone is in favor of primary hyperparathyroidism. About
85% of cases are caused by adenoma of a single gland, 15% are caused by hyperplasia of all 4
glands, and <1% are caused by parathyroid carcinoma.
In an older asymptomatic patient with serum calcium <12 mg/dL, conservative management is
an option. The only effective treatment for primary hyperparathyroidism is parathyroidectomy.
Many patients have a benign course over the years, but a major concern is the possibility of
progressive bone loss, increased risk of fractures, and recurrent nephrolithiasis.
Because this patient has a history of nephrolithiasis and persistently high calcium, surgery is
indicated. Surgery has high success rate with low morbidity and mortality.
Acute management of hypercalcemia is warranted when serum calcium >12 mg/dL or when
severe symptoms are present. The goal is to alleviate symptoms; it is not necessary to achieve
normal serum calcium levels. These measures allow time to complete diagnostic studies and
begin treatment of underlying conditions.
Parathyroidectomy (because of young age and history of kidney stones)
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