Indications for Anticoagulation in Patients With Prosthetic Heart Valves

All patients with mechanical valves require warfarin therapy. The risk of embolism is greater with a valve in the mitral position (mechanical or biological) than in the aortic position. With either type of prosthesis or valve location, the risk of emboli is higher in the first few days and months after valve insertion. Low-dose aspirin is recommended for all patients with prosthetic valves (see Table 1. For patients with mechanical valves, the addition of low-dose aspirin (80 to 100 mg/d) to warfarin therapy (INR 2.0 to 3.5) not only further decreases the risk thromboembolism but also decreases mortality due to other cardiovascular diseases. A slight increase in risk of bleeding with this combination should be kept in mind.
Recommendations for Antithrombotic Therapy in Patients With Prosthetic Heart Valves
Class I
1.First 3 months after valve replacement: Warfarin- INR 2.5 to 3.5
2.3 or more months after valve replacement:
A. Mechanical valve
AVR and no risk factor*:
Bileaflet valve or Medtronic Hall valve, Warfarin- INR 2 to 3
Other disk valves or Starr-Edwards valve, Warfarin- INR 2.5 to 3.5
AVR and risk factor,* Warfarin- INR 2.5 to 3.5
MVR, Warfarin- INR 2.5 to 3.5

B. Bioprosthesis
AVR and no risk factor,* Aspirin- 80 to 100 mg/d
AVR and risk factor,* Warfarin- INR 2 to 3
MVR and no risk factor,* Aspirin- 80 to 100 mg/d
MVR and risk factor,* Warfarin- INR 2.5 to 3.5

Class IIa
1.Addition of aspirin to warfarin: Aspirin- 80 to 100 mg daily
2.High-risk patients for whom aspirin cannot be used: Warfarin- INR 3.5 to 4.5
Class IIb
Starr-Edwards AVR and no risk factor,* Warfarin, INR 2 to 3

Class III
1.Mechanical valve, no warfarin therapy.
2.Mechanical valve, aspirin therapy only.
3.Bioprosthesis, no warfarin and no aspirin therapy.

Symptom and Sign Diabetes

SYMPTOMS AND SIGNS

Type 1 diabetes
Increased urination is a consequence of osmotic diuresis secondary to sustained hyperglycemia. This results in a loss of glucose as well as free water and electrolytes in the urine. Thirst is a consequence of the hyperosmolar state, as is blurred vision, which often develops as the lenses are exposed to hyperosmolar fluids.
Weight loss despite normal or increased appetite is a common feature of type 1 when it develops subacutely. The weight loss is initially due to depletion of water, glycogen, and triglycerides; thereafter, reduced muscle mass occurs as amino acids are diverted to form glucose and ketone bodies.
Lowered plasma volume produces symptoms of postural hypotension. Total body potassium loss and the general catabolism of muscle protein contribute to the weakness.
Paresthesias may be present at the time of diagnosis, particularly when the onset is subacute. They reflect a temporary dysfunction of peripheral sensory nerves, which clears as insulin replacement restores glycemic levels closer to normal, suggesting neurotoxicity from sustained hyperglycemia.
When absolute insulin deficiency is of acute onset, the above symptoms develop abruptly. Ketoacidosis exacerbates the dehydration and hyperosmolality by producing anorexia and nausea and vomiting, interfering with oral fluid replacement.
The patient's level of consciousness can vary depending on the degree of hyperosmolality. When insulin deficiency develops relatively slowly and sufficient water intake is maintained, patients remain relatively alert and physical findings may be minimal. When vomiting occurs in response to worsening ketoacidosis, dehydration progresses and compensatory mechanisms become inadequate to keep serum osmolality below 320–330 mosm/L. Under these circumstances, stupor or even coma may occur. The fruity breath odor of acetone further suggests the diagnosis of diabetic ketoacidosis.
Hypotension in the recumbent position is a serious prognostic sign. Loss of subcutaneous fat and muscle wasting are features of more slowly developing insulin deficiency. In occasional patients with slow, insidious onset of insulin deficiency, subcutaneous fat may be considerably depleted.

Type 2 diabetes
While many patients with type 2 diabetes present with increased urination and thirst, many others have an insidious onset of hyperglycemia and are asymptomatic initially. This is particularly true in obese patients, whose diabetes may be detected only after glycosuria or hyperglycemia is noted during routine laboratory studies. Occasionally, type 2 patients may present with evidence of neuropathic or cardiovascular complications because of occult disease present for some time prior to diagnosis. Chronic skin infections are common. Generalized pruritus and symptoms of vaginitis are frequently the initial complaints of women. Diabetes should be suspected in women with chronic candidal vulvovaginitis as well as in those who have delivered large babies (> 9 lb, or 4.1 kg) or have had polyhydramnios, preeclampsia, or unexplained fetal losses.
Obese diabetics may have any variety of fat distribution; however, diabetes seems to be more often associated in both men and women with localization of fat deposits on the upper segment of the body (particularly the abdomen, chest, neck, and face) and relatively less fat on the appendages, which may be quite muscular. Standardized tables of waist-to-hip ratio indicate that ratios of "greater than 0.9" in men and "greater than 0.8" in women are associated with an increased risk of diabetes in obese subjects. Mild hypertension is often present in obese diabetics. Eruptive xanthomas on the flexor surface of the limbs and on the buttocks and lipemia retinalis due to hyperchylomicronemia can occur in patients with uncontrolled type 2 diabetes who also have a familial form of hypertriglyceridemia.

PATHOLOGY OF ACUTE PANCREATITIS

PATHOLOGY
Detailed histological studies of pancreatic tissue are available from a limited number of cases of human acute pancreatitis. A histological spectrum of acute pancreatitis is recognized ranging from mild, interstitial disease to coagulation necrosis. 3 Interstitial pancreatitis may lead to local and systemic complications but is rarely fatal; necrotizing pancreatitis may be fatal in up to 30% of cases.

Interstitial
In interstitial pancreatitis the gland is edematous, but its gross architecture is preserved. Parenchymal inflammatory cells are present together with interstitial edema. Disruption of the normal acinar cell architecture is common and may contribute to the reduced enzyme secretion characteristic of acute pancreatitis. Zymogen granules are displaced from their fusion site in the apical domain of the cell and become dispersed throughout the cell, and the apical membrane appears contracted and microvilli disappear. 4 Zymogen granules fuse with each other instead of the apical membrane. Similar to animal models of pancreatitis, a distinct form of cell necrosis is observed in which the apical domain of the acinar cell is shed into the lumen, resulting in intact zymogen granules within the lumen. This pattern of partial cell necrosis may allow the acinus to regenerate rapidly after injury.

Necrotizing
Macroscopically, marked tissue necrosis and hemorrhage are apparent. Surrounding areas of fat necrosis are also prominent. These chalky areas of dead adipose tissue are found within the peripancreatic tissue and throughout the abdomen. Large hematomas often are located in the retroperitoneal space. The microscopic appearance of the pancreas parallels the gross changes, with marked fat and pancreatic necrosis. Vascular inflammation and thrombosis are common.