Protein-calorie malnutrition is associated with immunosuppression, poor wound healing, decreased basal metabolic rate, longer and more expensive hospital stays, and a higher mortality rate. Most otolaryngology patients are well nourished, but this is not the case with many head and neck cancer patients who have difficulty maintaining adequate oral intake to prevent weight loss. In the surgical patient, mild to moderate malnutrition is defined as an unintentional weight loss of 6% to 12% of the usual body weight in the preceding 3 to 6 months or 80% to 85% of ideal body weight. Severe malnutrition is suggested with weight loss greater than 12%, serum albumin less than 2.5 g/dL, serum prealbumin less than 5 mg/dL, serum transferrin less than 200 mg/dL, and decreased immune function manifested as total lymphocyte count less than 900 mm3
Patients with mild to moderate malnutrition may undergo most otolaryngology surgeries, with attention given to nutrition in the postoperative period; however, severe malnutrition should be treated with 7 to 10 days of nutritional replacement before elective surgery. The daily caloric requirement for most hospitalized adults is 25 to 35 kcal/kg of body weight. Protein is usually required at 0.5 to 1.0 g/kg/day, but the critically ill patient may need an increase to 1.5 to 2.0 g/kg/day. Daily caloric requirements (basal energy expenditure) can be estimated by formulas such as the Harris-Benedict scale, available in standard nutrition textbooks, although the values may have to be increased 1.25 to 1.5 times due to the stress of surgery. Because poor oral intake is presumed to have caused the malnutrition, most replacement therapy should be in the form of total parenteral nutritional (TPN) therapy or enteral feedings. Enteral feedings are preferable to TPN for several reasons, including providing more nutrients, less likelihood of hyperglycemia, promotion of immune function, elimination of a central catheter, buffering of gastric acid, and less expense (10
). Enteral feedings can be either a blenderized normal diet or a nutritionally complete commercial formula with an energy supply of 1 to 2 kcal/mL or higher. For nasogastric tubes, gravity bolus feedings are usually given at an initial rate of 50 to 100 mL every 4 hours, increasing to 240 to 360 mL every 4 hours. Continuous feedings may be preferable to bolus
since they constantly buffer gastric acid, reduce aspiration risk, and have smaller residual volumes. They can be started at 25 to 30 mL/h and increased after 24 hours by 25 mL/h until the target intake is reached. The limiting factors in the volume of tube feedings include vomiting, cramping, abdominal distention, and diarrhea. Because regurgitation or aspiration is a risk of tube feedings, residual gastric volume should be checked every 4 hours and before each tube feeding. A gastric residual volume of 300 to 400 mL may signal intolerance for gastric tube feedings. In patients with long-term nutritional needs, a percutaneous endoscopic gastrostomy or surgically placed jejunostomy tube often is required. Jejunal tubes require continuous peristaltic pump infusion at a slower rate and with isotonic solutions. In severely malnourished patients, caution must be used because of the “refeeding syndrome,” caused by a reactive hyperinsulinemia secondary to the sudden intake of glucose. Particular attention is paid to fluid overload and congestive heart failure, cardiac dysrhythmias, glucose intolerance, and electrolyte abnormalities such as hypophosphatemia, hypokalemia, and hypomagnesemia.
For patients who are unable to take nutrition by the gastrointestinal tract, replacement should be with TPN delivered through a central venous line. Consultation with the appropriate dietary service is essential. A common TPN solution has at least 1 kcal/mL and contains 500 mL each of 50% dextrose and 500 mL of 10% amino acids, with added vitamins, electrolytes, and trace elements. Fat emulsion composed of soybean or safflower oil as a 10% to 20% solution, 250 to 500 mL, can be given as little as weekly to supply essential fatty acids. The three components with additives can also be mixed in a 3-L bag, termed “3-in-1 solution,” and given over a 24-hour period and is often used to simplify administration. In general, the infusion is started with 1,000 mL in the first 24 hours and increased as tolerated to 2,000 mL/day. Two liters of solution provides at least 2,000 to 2,500 cal/day and essential nutrients. It is important in both enteral nutrition and TPN to provide enough water to prevent azotemia and hypernatremia. Some formulas now contain substances previously thought to be “nonessential” such as arginine, glutamine, and omega-3 fatty acids. These “immunonutrition” solutions have been found to decrease the incidence of infections.
The safety of TPN requires frequent monitoring. Vital signs and glucose should be monitored every 6 hours initially. When the patient is on a stable regimen, glucose, weight, caloric and protein intake, serum electrolytes, and blood urea nitrogen (BUN) can be checked twice weekly. Liver-function studies, serum magnesium, total protein, albumin, transferrin, triglycerides, complete blood count (CBC), prothrombin time (PT), and iron levels are measured weekly. Meticulous care of the central catheter is required to prevent catheter-site infection.
Tube feedings are withheld on the day of surgery. TPN is tapered before surgery and should not be given intra-operatively because of the risk of hyperglycemia. In the postoperative period, feeding as early as possible, either by mouth or tube feeding, is encouraged, and postoperative TPN should be used only if enteral feedings cannot be accomplished within 5 to 7 days after surgery. For tube feedings, water may be provided within hours of the termination of surgery, whereas full-strength formula at a rate of 30 mL/h can be started on the first postoperative day for most patients.
Blood Components and Transfusion
Specific indications for preoperative transfusion are discussed in the following sections (13
). Rapid correction of hematologic deficiencies usually depends on blood transfusions. Whole blood is rarely used; it is separated into its components for safety and efficiency (Table 3.1
). The broadest coverage for urgent surgery in patients with coagulation abnormalities is fresh frozen plasma (FFP), which contains all the clotting factors, although no platelets are present, and the fibrinogen level is low. Fibrinogen transfusion is no longer used because of the high risk of viral transmission; cryoprecipitate is used to treat low fibrinogen levels.
Serious complications to transfusions include immunemediated hemolytic reactions, anaphylactic reactions, and transmission of viral or bacterial disease. More recently, the immunosuppressive effect of the antigenic components of blood, termed immunomodulation, has been recognized (15
). Far more common are mild hypersensitivity and nonhemolytic febrile reactions. Pretreatment with an antihistamine (diphenhydramine, 50 mg) and acetaminophen usually minimizes such reactions and permits completion of the transfusion. Of specific concern is the patient who has undergone massive transfusion. Volume overload may be minimized by using packed red blood cells. Hyperkalemia, hypokalemia, hyperammonemia, and
acidosis require specific treatment. Massive transfusions may lead to significant thrombocytopenia and coagulation factor depletion. Clotting studies such as activated partial thromboplastin time (aPTT), PT or international normalized ratio (INR), which is PT corrected to an international standard, platelet counts, and fibrinogen levels should be monitored for any sign of coagulopathy. Hypothermia can be minimized by warming blood and crystalline replacement. Citrate toxicity can cause a decrease in ionized calcium. Replacement with calcium gluconate (10 mL, 10%, IV) is reserved for symptomatic hypocalcemia and is not given prophylactically.
TABLE 3.1 BLOOD COMPONENTS
Packed red blood cells
Acute hemorrhage, symptomatic anemia
Replace multiple coagulation deficits, specific coagulation deficits if factor concentrates unavailable
Quantitative and qualitative platelet disorders
Low fibrinogen, factor VIII, von Willebrand’s factor XIII
Specific factor deficits, especially VIII, IX, V
Immunoglobulin, high titer antibodies
Alternatives to transfusion should be considered pre-operatively. For elective surgery, the patient can be an autologous donor with a maximum of 1 U donated every 72 hours, up to 72 hours before surgery, as long as the patient maintains a hematocrit of greater than 33%. Autologous donation, however, is not cost-effective unless significant blood loss is anticipated. Other methods include isovolemic hemodilution (removal of whole blood preoperatively, replacement with crystalloid, and reinfusion after acute blood loss), intraoperative autotransfusion (return of processed blood from the operative field), or use of erythropoietin for several weeks preoperatively to stimulate red blood cell production.
A preoperative hemoglobin level should be obtained on all female patients but is not necessary in asymptomatic male patients younger than 50 years who do not have a history of bleeding or anemia. Anemia is significant because of the decreased oxygen-carrying capacity available during anesthesia (13
). The previous minimal acceptable hemoglobin level of 10 g/dL for surgery or transfusion has been lowered to 6 to 7 g/dL, which is adequate for tissue oxygen delivery if circulating volume is normal. Healthy patients or chronically anemic patients may undergo surgery safely at these levels if minimal blood loss is expected. Two situations may require transfusion: active bleeding and coronary artery disease. In the patient with coronary artery disease, the hemoglobin should be increased to 10 g/dL or hematocrit of 30% (15
) before surgery.
Elevated hemoglobin and hematocrit levels, respectively, greater than 16.5 g/dL and 55% in males and 15.3 g/dL and 52% in females also requires evaluation to exclude polycythemia or erythrocytosis (17
). The most common cause is a relative polycythemia caused by reduced plasma volume from conditions such as dehydration. Tests, such as an increased chromium 51 red cell mass and low erythropoietin levels, may point toward a diagnosis of Polycythemia vera, which is associated with a higher incidence of thrombotic and hemorrhagic perioperative complications. For elective surgery, the patient should ideally be stable for several months before surgery. A hematocrit of 45% can be obtained with phlebotomy by removing 125 to 200 mL of blood every other day in healthy individuals, and slower removal in older patients or patients with cardiac disease. Platelet counts should ideally also be reduced to less than 500,000. In the emergency situation, whole blood can be removed and replaced with crystalloid.
Two hemoglobinopathies are of concern. The first is sickle cell disease. Sickle cell trait is not associated with increased surgical risk. In patients with the homozygous condition, the level of hemoglobin S should be reduced to avoid sickling crisis or acute chest syndrome during anesthesia or during the postoperative period. The simplest method is to transfuse to a hemoglobin level of 10 g/dL before surgery. Hypoxia, hypernatremia, hypothermia, acidosis, and volume depletion should be avoided. Hypotonic fluids should be given to decrease blood viscosity (17
). The second hemoglobinopathy is glucose-6-phosphate dehydrogenase deficiency, which causes oxidant damage to hemoglobin within erythrocytes and is almost exclusively seen in men. Preoperative screening for this deficiency should be performed if a family history of the deficiency or unexplained hemolysis exists. The condition is not a risk for surgery, but certain medications should be avoided in the postoperative period to minimize the risk of hemolysis.
Thrombocytopenia is defined as a platelet count of less than 140,000/mL (13
). For otolaryngologic surgery with minimal anticipated blood loss, a platelet count of 20,000/mL may be sufficient, but the platelet count should be 50,000/mL for more major surgery. Each unit of platelets for transfusion will increase the platelet count 5,000 to 10,000/mL, and the platelet half-life is usually 2 to 3 days, unless increased destruction occurs. Ideally, the platelet count should be maintained above 20,000/mL for 3 to 4 days postoperatively. Thrombocytopenia developing in the postoperative period is unusual unless massive transfusion has been necessary, but sepsis, disseminated intravascular coagulation (DIC), and drug-induced thrombocytopenia must be considered.
Qualitative platelet disorders with abnormalities in platelet function may exist even with a normal platelet count. Platelet dysfunction may be present if a patient has a history of uremia or dialysis, liver disease, von Willebrand disease (vWD), abnormal bleeding from previous surgery, or with a recent history of ingestion of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), or other medicine, such as penicillin, that may affect platelet function. Aspirin is the most potent of the cyclooxygenase (COX) inhibitors, and irreversibly inhibits platelets for 5 to 7 days. Other NSAIDs, such as ibuprofen, are competitive inhibitors, and the platelet dysfunction can be reversed with desmopressin acetate (DDAVP). The selective COX-2 inhibitors, such as celecoxib, in usual doses do not cause platelet dysfunction. Thienopyridine class agents, such as clopidogrel, and glycoprotein 2b/3a receptor inhibitors, such as abciximab,
prevent platelet aggregation, and are not reversible. Tests for qualitative platelet dysfunction can be considered. In the past, a bleeding time was performed, but this test is now considered a global screening test, is often inadequate to identify many causes of platelet dysfunction, and is not useful as a predictor of bleeding during surgery. Current evaluation includes tests for platelet aggregometry, membrane glycoproteins, capillary tube shear testing, and should include screening for deficiency in von Willebrand factor (vWF), necessary for platelet adhesiveness. DDAVP may reverse the action of some platelet inhibitors such as NSAIDs or elevated BUN, may increase vWF, and may partially reverse the platelet dysfunction. Platelet transfusions or administration of DDAVP should be performed if emergency surgery is necessary. In elective surgery, medications causing platelet dysfunction should be stopped between 4 and 10 days before surgery, except in certain conditions such as the recent insertion of drug eluting cardiac stents.
Disorders of Hemostasis
The yield of routine preoperative coagulation studies, such as PT, aPTT, and platelet counts, is quite low unless the patient’s history indicates a bleeding problem. This history should be searched carefully for congenital or acquired abnormalities of bleeding (18
) (Table 3.2
The perioperative management of patients receiving anticoagulant therapy requires specific comment. Heparin augments the effects of antithrombin (previously termed antithrombin III), which inhibits clotting enzymes, specifically factor Xa and thrombin (20
). Low-molecular-weight heparins (LMWHs), such as enoxaparin, are increasingly used for deep venous thrombosis (DVT) prevention andginactivate factor Xa more than thrombin. LMWH has several advantages over heparin, including less risk of heparin-induced thrombocytopenia, longer subcutaneous injection half-life, and less necessity for monitoring anticoagulant effect. Warfarin, the most common anticoagulant, is given orally and is a vitamin K antagonist that decreases production of vitamin K-dependent clotting factors. Direct thrombin inhibitors, such as bivalirudin, are irreversible, but may cause less bleeding than heparin, so are preferred during procedures such as percutaneous coronary angioplasty. The need for anticoagulation should be discussed with the patient’s primary care physician, and the method of preoperative discontinuation of the anticoagulant should be based on the estimated risk of DVT, pulmonary embolism (PE), or stroke (19
). Patients in a low-risk category may simply have warfarin discontinued 2 to 3 days before surgery and restart it after surgery. Low-risk patients include those with aortic valve prosthesis or a resolved cause of a previous DVT. High-risk patients, such as those with a history of emboli of cardiac origin, atrial fibrillation, or mitral valve disease or prosthesis, should have warfarin discontinued several days before surgery and replaced with heparin. Intravenous heparin should be used to increase the aPTT to 1.5 to 2 times normal levels. Twelve hours before surgery, heparin should be discontinued, and the PTT will return to normal by the time of surgery. The effect of warfarin may be counteracted with vitamin K administration, as indicated in Table 3.2
TABLE 3.2 DISORDERS OF HEMOSTASIS
Hemophilia A (VIII)
Factor VIII concentrate or recombinate VIII, FFP, CP
Minor defect: DDAVP
vWD (VIII, vWF)
DDAVP (except type 2B vWD)
Intermediate purity factor VIII with high vWF
Hemophilia B (IX)
Factor IX or recombinate IX concentrate (preferred)
FFP (note: CP does not contain IX)
Rapid reversal: vitamin K, 10 mg, SC or IV, q12h × 3 days
Vitamin K deficiency
FFP 2-4 U Monitor dose with PT or INR
Protamine, 1 mg neutralizes 100 U heparin (avoid overcorrection—monitor aPTT)
FFP, CP, platelets
FFP, fresh frozen plasma; CP, cryoprecipitate; aPTT, activated partial thromboplastin time; PT, prothrombin time; INR, international normalized ratio; DIC, disseminated intravascular coagulation; vWD, von Willebrand’s Disease.
If surgery is imminent in a patient after anticoagulation with a warfarin product, 2 to 4 U of FFP may be given to correct the coagulation-factor deficiencies immediately while vitamin K takes effect. Repeated PT or INR tests should be
performed to evaluate the results of therapy. If an emergency situation arises in the heparinized patient, either with unfractionated heparin or LMWH, protamine sulfate may be given to antagonize heparin immediately. Unlike heparin, however, LMWH is only partially reversed with the administration of protamine making it less safe in patients at high risk of bleeding (15
). Caution, however, should be used in the administration of protamine because it can induce a hypercoagulable state. On the one hand, it is crucial to note that FFP will not correct the coagulation defect caused by heparin. On the other hand, reversal of direct thrombin inhibitors must be accomplished by infusion of FFP.
The timing for restarting anticoagulants postoperatively depends on patient risk factors for thrombosis and embolization and on the type of surgery and hemostasis obtained at surgery. In neurotologic surgery and possibly airway surgery in which bleeding would present a life-threatening problem, anticoagulation should be delayed at least 36 to 48 hours. Rapid anticoagulation then is accomplished with intravenous heparin, whereas slower anticoagulation is accomplished simultaneously by restarting oral warfarin.
Intraoperative and Postoperative Bleeding
When the cause of intraoperative or postoperative bleeding is not an unsecured vessel, a search must be made for a coagulation disorder (15
). Screening tests include CBC (hemoglobin, hematocrit, platelet count, and morphology), PT (INR), aPTT, qualitative platelet tests as noted earlier, and fibrinogen. Further testing and treatment depend on the findings of these preliminary tests as follows (15
Normal PT and aPTT: The most common abnormality is impaired platelet activity, either thrombocytopenia or platelet dysfunction. Treatment is with platelet transfusion or DDAVP, as previously discussed. Other causes include factor XIII or fibrinogen deficiency.
Normal PT, abnormal aPTT: Drug-induced effect (heparin), vWD, or clotting factor deficiency, such as hemophilia, should be suspected and treated as noted earlier.
Abnormal PT and normal aPTT: Present with liver disease or warfarin anticoagulation, treated with vitamin K and FFP administration.
Both PT and aPTT abnormal: The first step is to repeat aPTT and PT testing to exclude laboratory error. If this is not present, then severe reductions in multiple clotting factors are present, and severe malnutrition with depleted vitamin K-dependent clotting factors, DIC, severe hemodilution, or nephrotic syndrome may be present.
Hemodilution and nephrotic syndrome coagulopathy is caused by decreased concentration of clotting factors, whereas DIC is the result of consumption of clotting factors. Moderate DIC initiates intravascular microthrombi, which lodge in critical organs and can produce adult respiratory distress syndrome or renal and hepatic failure. Severe DIC occurs when the intravascular microthrombi trigger an overwhelming fibrinolytic response and resultant dissolution of previously formed clots, leading to bleeding. The bleeding in DIC is the result of a cycle of clot formation and fibrinolysis, leading to consumption of clotting factors. In addition to the routine coagulation tests, a search is made for the presence of fibrin split products and D-dimer, the latter produced when plasmin acts on crosslinked fibrin. A high D-dimer level, especially greater than 2,000 ng/mL, is presumptive evidence of DIC (21
). Treatment of DIC in the past had included the use of heparin to stop the clotting and allow return of clotting factors to more normal levels. Current recommendations for treatment are to remove the clotting stimulus (e.g., dead tissue, abscess), correct hypothermia, and correct blood loss with packed red cells and clotting factors with FFP and platelets.
DVT and PE are significant postoperative problems (17
). Major risk factors are immobilization, history of thromboembolic disease, varicose veins, oral contraceptives and estrogen compounds, age older than 40 years, malignancy, central venous catheters, antiphospholipid syndrome, and hypercoagulable states such as erythrocytosis, thrombocytosis, and inherited thrombophilic disorders such as Leiden factor V mutation, prothrombin 20210 mutation, and deficiencies of substances antithrombin III, protein C, and protein S, which results in decreased lysis of clots.
Mechanical preventive measures usually are used first in otolaryngology patients. Any method designed to increase lower-extremity blood return is helpful. Traditional measures include early mobilization, leg elevation, elastic stockings, and physical therapy. A newer innovation is the external pneumatic compression boot, which is applied to the calf and thigh. The boot is intermittently inflated, the pressure held, and then deflated to massage blood up from the lower extremity. They should be considered for any patient who may not be mobilized early or who is undergoing a neurotologic, neurosurgical, or airway procedure in which prophylactic anticoagulation may not be indicated. Caution is used in patients with severe peripheral arterial vascular disease because vascular supply to the lower extremity may be compromised.
The pharmacologic methods of prevention of thromboembolic complications, such as heparin or warfarin, are quite effective, but they require starting the patient on treatment before surgery, which increases the risk of bleeding during surgery. The traditional use of heparin, 5,000 U, twice daily, in the perioperative period has been replaced by different protocols: (a) an adjusted dose of unfractionated heparin IV or SC to increase the aPTT by 2 to 3 seconds; or (b) LMWH, such as enoxaparin, 1 mg/kg,
q12h; (c) a factor Xa inhibitor, such as fondaparinux, 2.5 to 5 mg daily for adults greater than 50 kg., or (d) warfarin to increase the INR to 2-3.
Despite preventive measures, DVT and subsequent PE may develop (22
). The diagnosis is difficult, but PE should be suspected in patients with sudden onset of tachypnea, dyspnea, chest pain, hemoptysis, hypoxia, delirium, or dysrhythmias. For patients at risk for PE where no contra-indication exists, anticoagulation should be started while testing is performed. If significant clinical suspicion exists, further studies can include contrast-enhanced spiral computed tomography (CT) scan combined with a CT venogram of the pelvis and leg, a ventilation-perfusion (VQ) scan, magnetic resonance angiography, or pulmonary angiography. If the pulmonary CT scan shows one or more luminal filling defects, especially bilateral, the diagnosis of PE is almost certain (21
). Conversely, if the VQ scan is normal, there is little chance of a PE. Pulmonary angiography is performed in high-risk patients with equivocal test results.
If no contraindication exists, anticoagulation is necessary in all patients with proximal DVT and PE (23
). In neurotologic, skull base, or procedures in the airway, the risk of bleeding must be considered. In other cases, heparin should be given immediately and continued for a minimum of 5 days, with the aPTT maintained in a range of 1.5 to 2 times control, while oral warfarin anticoagulant therapy is initiated to therapeutic levels. If the PE is massive, streptokinase, urokinase, or recombinant tissue plasminogen activator should be considered as thrombolytic therapy. Inferior vena caval interruption is used when anticoagulation is contraindicated or recurrent emboli are found in adequately anticoagulated patients.
Hyperglycemia is defined as a fasting blood glucose (BG) level greater than 126 mg/dL, a pre-meal BG greater than 140 mg/dL, a random BG greater than 180 mg/dL, or a 2-hour glucose tolerance test glucose greater than 200 mg/dL (24
). Multiple studies, both medical and surgical, have shown substantial increases in complications and mortality of hyperglycemic hospitalized patients (24
Approximately half of intensive care unit (ICU) patients and one-third of all hospitalized patients will be hyperglycemic during their hospitalization. Tight diabetic control is a challenge even for patients undergoing minor otolaryngology procedures and is critical in major procedures with prolonged hospital recoveries. Surgery and anesthesia increase production of stress hormones and worsen hyperglycemia.
Bedside capillary point of care (POC) testing is now the preferred method of BG monitoring as opposed to laboratory BG testing. Use of sliding scale insulin administration, which is a set amount of insulin for a given BG, is no longer recommended. A measurement of HbA1c aids in assessing average blood levels of glucose over the preceding 1 to 2 months. Oral hypoglycemic and non-insulin injectable antidiabetic medications are discontinued on admission. Insulin is the preferred method to achieve glycemic control in hospitalized patients. Recent recommendations use the concept of basal intermediate or long acting insulin once or twice daily with bolus rapid-acting or regular insulin before meals and at bedtime based on POC glucose testing (See Table 3.3
). Patients who are not eating or on enteric nutrition have bolus insulin based on POC glucose testing every four to six hours. Supplemental “corrective” short or rapid acting insulin is given for BG levels above the pre-meal target of 140 mg/dL or random BG of 180 mg/dL (24
). In the perioperative period, all insulin-dependent diabetics receive basal/bolus treatment, while Type 2 non-insulin dependent diabetics can have insulin treatment initiated based on BG measurements. Type 1 diabetics require insulin, even if fasting, to prevent severe hyperglycemia and ketoacidosis. Insulin is given subcutaneously (sc) as opposed to an IV bolus in hospitalized patients. Similarly, in surgery, the trend is away from IV bolus to either sc or continuous insulin infusion pumps. Tighter control of glucose levels requires close observation to prevent hypoglycemia, defined as BG less than 70 mg/dL. It is important that diabetics receive 3 g/kg of body weight each day of
carbohydrates to prevent protein catabolism and lipolysis. Dextrose 5% in water at 100 mL/h provides 5 g glucose per hour.
TABLE 3.3 MANAGEMENT OF SURGICAL PATIENTS WITH HYPERGLYCEMIA
Basal-Bolus Insulin Treatment
Total daily insulin dose: 0.5 units insulin/kg × weight in kg
0.2-0.4 units/kg in renal insufficiency, elderly, and lean patients
Example: Weight = 72 kg
72 kg × 0.5 = 36 units insulin
Basal dose (long acting, e.g., glargine insulin) = 18 units
Example: Given once daily in AM or split twice daily
Bolus dose (short or rapid-acting insulin) = 18 units in 3 divided doses
Example: 6 units given before each meal
Corrective dose = Short or rapid-acting insulin given in addition to the bolus dose for BG above optimal levels
Example: Initial 2-6 units while basal and bolus doses adjusted
Long-term management of poorly controlled patients is complex and best managed by the endocrinologist and multispecialty diabetic team. The otolaryngologist should know, however, basic management of postoperative increases in glucose. The most severe postoperative exacerbation is diabetic ketoacidosis (DKA) and is a true medical emergency with marked dehydration secondary to osmotic diuresis, hyperventilation in reaction to metabolic acidosis, and decreased levels of consciousness. The patient should be managed in the ICU. Immediate laboratory tests should include glucose (fingerstick or blood); potassium; serum ketones; other electrolytes such as magnesium, calcium, and phosphate; and blood gases to document the level of acidosis. All are repeated every 1 to 2 hours until the patient is stable, glucose is less than 250 mg/dL, and ketones have resolved. Cardiac monitoring is accomplished to exclude ectopy. Normal saline is given empirically over 20 to 30 minutes for volume repletion while test results are pending. The treatment of DKA is to give rapid-acting IV insulin, 10 to 15 U or 0.1 to 0.15 U/kg followed by the same dose hourly or via infusion pump. It is crucial, however, that potassium levels be determined and potassium replacement started at 10 to 40 mEq/h concurrently or before insulin to avoid profound hypokalemia, which can result from insulin facilitation of intracellular movement of potassium. The goal is to reduce the glucose level 50 to 75 mg/dL/h until the glucose level is 250 mg/dL.
In the less emergent situation, regular insulin is given at a dose of 4 to 10 U subcutaneously every 4 to 6 hours. Alternatively, a constant regular insulin infusion can be administered with a loading dose of 0.1 to 0.2 U/kg, followed by an infusion rate of 0.1 U/kg/h in a 0.9% sodium chloride solution. Blood glucose levels are measured every 1 to 2 hours. The patient then may be monitored during surgery in the same way as the well-controlled diabetic. Hyperosmolar nonketotic syndrome, characterized by hyperglycemia and dehydration, primarily requires restoration of intravascular volume and lower doses of insulin (0.05 to 0.15 U/kg/h). Discharge insulin or oral hypoglycemic agent dose depends on glucose control at the end of the patient’s hospitalization.
Thyroid and Parathyroid Disorders
Patients with mild to moderate hypothyroidism may undergo emergency surgery with little increase in morbidity. For elective surgery, gradual replacement of hormone is preferred because rapid repletion can lead to relative adrenal insufficiency and angina in patients with coronary insufficiency. Synthetic levothyroxine, with a usual daily dose of 0.1 to 0.2 mg (1.8 mcg/kg/day), is the preferred replacement medication and may be given orally or intravenously in the same dose (30
). The patient with severe hypothyroidism may have low temperature, hypotension, hyponatremia, hypoventilation, and hypoglycemia. Severe hypothyroidism can have an initial presentation postoperatively, especially in the elderly. Whether present in the preoperative patient needing urgent surgery or developing in the postoperative period, severe hypothyroidism can be treated with IV thyroxin, 200 to 500 mcg. Hydrocortisone, 100 mg IV every 12 hours, also should be given because adrenocorticotropin pituitary responsiveness to stress may be decreased (31
). Hydrocortisone is continued until serum cortisol can be evaluated and pituitary responsiveness checked. Although fluid volume must be restored, free water clearance is diminished. Care must be taken with hypotonic intravenous solutions to avoid hyponatremia and water intoxication.
Elective surgery in hyperthyroid patients should be delayed, if possible, until the patient is in a euthyroid state. If urgent surgery must be performed in the thyrotoxic patient, iodines, propranolol, and thionamide antithyroid drugs, such as propylthiouracil (PTU) or methimazole,
should be used to reduce the risk of thyrotoxic crisis (30
). PTU blocks thyroid hormone production, inhibits the conversion of thyroxine (T4) to triiodothyronine (T3), and usually is given in an oral dose of 100 to 200 mg three times daily. Methimazole is given either as divided doses of 10 mg every 8 to 12 hours, or as a single 20- to 40-mg daily dose. In the routine treatment of thyrotoxicosis, methimazole is preferred to PTU because fewer adverse reactions occur, especially PTU-induced hepatitis, and compliance is potentially higher with a single daily dose. PTU is preferred in pregnancy and the treatment of thyroid storm, the latter due to PTU blockage of extrathyroidal deiodination of T4 to T3. Iodides induce a transitory inhibition of thyroid hormone production and release from the gland and decrease vascularity of the gland, which lasts 10 to 14 days. Iodides can be given as a saturated solution of potassium iodide at a dose of 5 drops orally every 6 hours or Lugol’s solution, 10 drops, three times daily. Palpitations, tachycardia, and tremor can be controlled with a beta-blocker such as propranolol in an initial dose of 20 to 40 mg, taken orally four times daily or 1 to 2 mg, given intravenously every 4 to 6 hours. Hydrocortisone should be given to counter relative adrenal insufficiency. Replacement thyroxine should be given postoperatively, and a thyroid-stimulating hormone and T4
checked 6 to 12 weeks after surgery.
Thyrotoxic crisis, or thyroid storm, manifests by severe exaggeration of the classic symptoms of thyrotoxicosis and may develop intraoperatively or in the immediate postoperative period (30
). The patient may have a marked fever, sweating, tachycardia, vomiting, abdominal pain, and delirium. Large doses of the same medications are given (Table 3.4
). In the treatment of thyrotoxic crisis, the order of medical therapy is important. Although iodide blocks release of thyroid hormone, it also is the precursor for oxidation to iodine. For this reason, PTU is given first to prevent this oxidation used in hormone production, and then, at least 30 minutes later, iodide is given to block hormone release. Supportive therapy includes temperature control with acetaminophen or a cooling blanket. Sedation and oxygen therapy may be needed, and the patient should receive adequate glucose-containing intravenous solutions because of the high metabolic rate. Aspirin is contraindicated since it binds to thyroid binding globulin and displaces T4, increasing the available hormone.
TABLE 3.4 MEDICAL CONTROL OF THYROTOXIC CRISIS
Propylthiouracil, 200 mg, q4h or methimazole, 30 mg, q6h
Sodium iodide, 500 mg, IV, twice daily
Propranolol, 1-2 mg/min (total 10 mg) or 40-80 mg, PO, q6h, prn pulse >100
Dexamethasone, 4 mg, q6h, or hydrocortisone, 100 mg, IV, q6h
Replacement of volume deficit
Treatment of infections
Hypocalcemia, defined as a serum level less than 9 mg/dL if albumin is normal, may develop in any person undergoing parathyroid or bilateral thyroid surgery (32
). After surgery, serum calcium and phosphate levels should be determined every 6 to 8 hours for the first several days, followed by daily levels thereafter. Serum ionized calcium alone is the optimal single measure if albumin levels are uncertain (31
). If the calcium level decreases to less than 7.0 mg/dL, signs or symptoms of latent tetany should be sought. A positive Chvostek or Trousseau sign, hyper-reflexia, numbness or tingling in the extremities, or circumoral paresthesias are indications to begin calcium replacement. Oral replacement can be accomplished with calcium carbonate, 250 to 500 mg, orally, four times daily, and vitamin D3
, 0.25 to 2.00 mg, orally, daily.
Laryngeal stridor, overt tetany, or seizures are medical emergencies and require IV calcium replacement. Calcium gluconate (10%) is less irritating than calcium chloride and is given as one to two ampules (10 to 20 mL) diluted in 50 to 100 mL of dextrose solution infused over a 10-minute period. Each ampule contains 1 g of calcium gluconate and 93 mg of elemental calcium. This emergency infusion of calcium gluconate can be repeated every 15 to 20 minutes, followed by a continuous infusion. The infusion can be prepared with six ampules of 10% calcium gluconate (540 mg elemental calcium) in 500 mL of D5W given at 1 mL/kg/h, giving approximately 1 mg/kg/h of elemental calcium (34
). Deficiencies in magnesium, sodium, and albumin must be corrected. Overly rapid replacement of calcium can potentiate digitalis toxicity in cardiac patients. Hyperventilation in an anxious patient will cause a respiratory alkalosis with resultant worsening of the hypocalcemia. Patients with prolonged hypocalcemia may require oral calcium carbonate or calcium citrate replacement with 1.5 to 3 g each day of elemental calcium and vitamin D.