co-exist disease and anesthesiology

1. DIABETES MELLITUS
Signs and Symptoms
TYPE 1 DIABETES
10% of all cases of diabetes are type 1
diagnosed before the age of 40
caused by a T cell–mediated autoimmune
destruction of beta cells in the pancreas.

2. At least 80% to 90% of beta cell function must
be lost before hyperglycemia occurs.
presentation is ofen sudden and severe
hyperglycemia over several days to weeks
associated with fatigue, weight loss, polyuria,
polydipsia, blurring of vision, and signs of
intravascular volume depletion.

3. diagnosis is based on the presence of a random blood
• BS more than 200 mg/dL
• Hb A1c level of more than 7.0%.
• Te presence of ketoacidosis
TYPE 2 DIABETES
90% of all cases of diabetes mellitus in the world.
the middle to older age group
Type 2 diabetes is characterized by relative beta cell insuffciency
and insulin resistance

4. Tree important defects :
(1) an increased rate of hepatic glucose release
(2) impaired basal and stimulated insulin secretion
(3) inefcient use of glucose by peripheral tissues (i.e., insulin resistance)
Impaired glucose tolerance is associated with an increase in body
weight, a decrease in insulin secretion, and a reduction in peripheral
insulin action.
Metabolic syndrome : combines insulin resistance with hypertension,
dyslipidemia, a procoagulant state, and obesity, and is associated with
premature atherosclerosis and subsequent cardiovascular disease.

5. Diagnosis
upper limit for normal fasting glucose level is 100 mg/dL.70-100
Any fasting glucose level between 101 and 125 mg/dL is impaired fasting glucose.
The Hb A1c test provides a valuable measure of long-term glycemic control 60-90 days.
The normal range for Hb A1c is 4% to 6%.

8. Treatment
type 2 diabetes are dietary With weight loss,
exercise therapy, and oral antidiabetic drugs.
Oral agents:
Hypoglycemia is the most common side efect.
sulfonylureas :ATP channels in the myocardium
mediate ischemic preconditioning, which results in
larger myocardial infarction areas.

9. Not only must hyperglycemia be treated but all abnormalities of insulin
resistance (metabolic syndrome) must be managed, with the goals of therapy
including an Hb A1c level of less than 7%, a low-density lipoprotein
level of less than 100 mg/dL, a high-density lipoprotein level of more
than 40 mg/dL in men and more than 50 mg/dL in women, a
triglycerides level of less than 200 mg/dL, and a blood pressure of less
than 130/80 mm Hg.
INSULIN
type 1 diabetes and 30 % of patients with type 2 diabetes
total daily basal dose of insulin equals ( weight × 0.3), with the hourly rate
obtained by dividing by 24.

10. Hypoglycemia is the most frequent and dangerous
complication of insulin therapy.
exacerbated by simultaneous administration of alcohol,
sulfonylureas ,biguanides, thiazolidinediones, angiotensin-
converting enzyme (ACE) inhibitors, monoamine oxidase
inhibitors, and nonselective β-blockers.

11. .Hypoglysemia The diagnosis in adults requires a plasma
glucose level of less than 50 mg/dL.
Symptoms are adrenergic (sweating ,tachycardia,
palpitations, restlessness, pallor) and neu-roglycopenic
(fatigue, confusion, headache, somnolence ,convulsions,
coma).
Treatment includes the administration of sugar and
 glucose 0.5 g/kg IV
 glucagon 0.5 to 1.0 mg IV, IM, or SC

12. Complications
1.DIABETIC KETOACIDOSIS
Diabetic ketoacidosis (DKA) is a complication of decompensated diabetes mellitus.
signs and symptoms of DKA are primarily the result of abnormalities in carbohydrate and
fat metabolism.
Episodes of DKA occur more commonly in patients with type 1 diabetes and are precipitated
by infection or acute illness.
signifcant osmotic diuresis with marked hypovolemia.
DKA results in an excess of glucose counterregulatory hormones, with glucagon activating
lipolysis and free fatty acids providing the substrate for ketogenesis.

13. An increase in production of ketoacids (β-hydroxybutyrate,
acetoac-etate, acetone) creates an anion gap metabolic
acidosis.
Substantial defcits of water, potassium, and phosphorus exist,
although laboratory values of these electrolytes may be normal or
increased.
Hyponatremia results from the efect of hyperglycemia and
hyperosmolarity on water distribution.
Te defcit of potassium is usually substantial (3 to 5 mEq/kg), and
the defcit of phosphorus can lead to diaphragmatic and skeletal
muscle dysfunction and impaired myocardial contractility.

14. The treatment of DKA consists
 administration of large amounts of normal saline
 efective doses of insulin
 electrolyte supplementation.
 1-intravenous loading dose of 0.1 unit/kg of regular insulin plus a low-
dose insulin infusion of 0.1 unit/kg/hr is initiated.
 2-Insulin administration must be continued until a normal acid-base
status is achieved.
 3-The insulin rate is reduced when hyperglycemia is controlled, the blood
pH is higher than 7.3, and bicarbonate level is more than 18 mEq/L.

15. 4- Potassium and phosphate are replaced with KCl and K2PO4.
5-Magnesium is replaced as needed.
6-Sodium bicarbonate is administered if the blood pH is less
than 7.1 .
cerebral edema can result from correction of hyperglycemia without
simultaneous correction of serum sodium level.
The overall mortality rate from DKA is 5% to 10%,

16.  HYPERGLYCEMIC HYPEROSMOLAR SYNDROME
 Hyperglycemic hyperosmolar syndrome is characterized by severe
hyperglycemia, hyperosmolarity, and dehydration.
 It usually occurs in patients with type 2 diabetes who are older than 60 years
of age in the context of an acute illness.
 The syndrome evolves over days to weeks with a persistent glycosuric
diuresis.
 When the glucose load exceeds the renal tubular maximum for glucose
reabsorption, a massive solute diuresis occurs with total body water
depletion.
 Te patient experiences polyuria, polydipsia, hypovolemia, hypotension,
tachycardia ,and organ hypoperfusion. Hyperosmolarity (>340 mOsm/L) is
responsible for mental obtundation or coma .

17.  Treatment : includes signifcant fluid resuscitation, insulin administration,
and electrolyte supplementation.
 1- If the plasma osmolarity is greater than 320 mOsm/L, large volumes of
hypotonic saline (1000 to 1500 mL/hr) should be administered until the
osmolarity is less than 320 mOsm/L, at which time large volumes of isotonic
saline (1000 to 1500 mL/hr) can be given.
 2- Insulin therapy is initiated with an intravenous bolus of 15 units of regular
insulin followed by a 0.1 unit/kg/hr infusion. Te insulin infusion is decreased to
2 to 3 units/hr whenthe glucose level decreases to approximately 250 to 300
mg/dL .
 The mortality rate of hyperglycemic hyperosmolar syndrome is 10% to 15%.

18.  MICROVASCULAR COMPLICATIONS
 nephropathy
 The clinical course is characterized by hypertension, albuminuria, peripheral edema, and a
progressive decrease in glomerular fltration rate.
 When the glomerular fltration rate decreases to less than 15 to 20 mL/min, the ability of
the kidneys to excrete potassium and acids is impaired and patients develop hyperkalemia
and metabolic acidosis.
 Hypertension, hyperglycemia, hypercholesterolemia, and microalbuminuria accelerate the
decrease in the glomerular fltration rate.
 Treatment of hypertension can markedly slow the progression of renal dysfunction. ACE
inhibitors are particularly benefcial in diabetic patients because they retard the progression
of proteinuria and the decrease in glomerular fltration rate.

19.  Peripheral Neuropathy
 A distal symmetric diffuse sensorimotor polyneuropathy is the
most common form.
 "stocking and glove" distribution.
 Retinopathy
 Diabetic retinopathy results from a variety of microvascular
changes
 Strict glycemic control and blood pressure control can reduce
the risk of development and progression of retinopathy.

20. Autonomic Neuropathy
Symptomatic autonomic neuropathy is rare and is present in fewer than 5%of diabetics.
Diabetic autonomic neuropathy can afect any part of the
autonomic nervous system and is the result of damaged
vasoconstrictor fibers, impaired baroreceptor function, and
ineffective cardiovascular reactivity.
Resting tachycardia and loss of heart rate variability during deep breathing.
A heart rate that fails to respond to exercise is indicative of signifcant cardiac
denervation and is likely to result in substantially reduced exercise tolerance.
.

21. systolic and diastolic dysfunction with a reduced
ejection fraction.
Dysrhythmias may be responsible for sudden
death.
In advanced stages, severe orthostatic
hypotension is present

22. The presence of cardiovascular autonomic neuropathy can be demonstrated by measuring
orthostatic changes in heart rate and blood pressure and the
hemodynamic response to exercise.
symptomatic patients will have nausea, vomiting, early satiety, bloating, and
epigastric pain. Treatment of gastroparesis includes strict blood glucose control,
consumption of multiple small meals, reduction of the fat content of meals, and use of
prokinetic agents such as metoclopramide.
Diarrhea and constipation are also common among diabetic patients and may be
related to diabetic autonomic neuropathy.

23. 1. the preoperative evaluation should emphasize the cardiovascular, renal, neurologic,
and musculoskeletal systems.
2. The index of suspicion should be high for myocardial ischemia and infarction. Silent
ischemia is possible if autonomic neuropathy
3. autonomic neuropathy predisposes the patient to perioperative dysrhythmias and
intraoperative hypotension.
1. Preoperative evaluation of the musculoskeletal system should look for limited joint
mobility caused by nonenzymatic glycosylation


24. 1. Firm, woody, nonpitting edema of the posterior neck and upper back
(scleredema of diabetes) coupled with impaired joint mobility may limit
range of motion of the neck and render endotracheal intubation difcult.
2. Gastroparesis may increase the risk of aspiration
 Management of insulin in the preoperative period.
 If a patient takes subcutaneous insulin each night at bedtime, two thirds of
this dose (NPH and regular) should be administered the night before surgery,
and one half of the usual morning NPH dose should be given on the day of
surgery. The daily morning dose of regular insulin should be held

25.  If the patient uses an insulin pump, the overnight rate should be
decreased by 30%.

 Oral hypoglycemics should be discontinued 24 to 48 hours
preoperatively.

 It is advised that sulfonylureas be avoided during the entire
perioperative period, because they block the myocardial
potassium ATP channels that are responsible for ischemia and
anesthetic-induced preconditioning.


26.  Aggressive glycemic control is important intraoperatively .
 Ideally, a continuous infusion of insulin should be initiated at least 2 hours before surgery.
 Intraoperative serum glucose levels should be maintained between 120 and 180 mg/dL.
 Levels above 200 mg/dL are likely to cause glycosuria and dehydration and to inhibit phagocyte function and
wound healing.
 Typically, 1 unit of insulin lowers glucose approximately 25 to 30 mg/dL.
 A typical rate is unit/kg/hr.
 An insulin infusion can be prepared by mixing
(1 unit/mL).

27.  Insulin infusion requirements are higher or patients undergoing
 coronary artery bypass graf surgery
 patients receiving steroids
 patients with severe infection
 patients receiving hyperalimentation
 patients receiving vasopressor infusions
 An insulin infusion should be accompanied by an
1. infusion of 5%dextrose in
2. half-normal saline
3. 20 mEq KCl
4. at 100 to 150 mL/hr

28.  Serum glucose level should be monitored at least every hour and even every 30
minutes in patients undergoing coronary artery bypass surgery or patients with
high insulin requirements.
 Urine glucose monitoring is not reliable.
 Avoidance of hypoglycemia is especially critical, since recognition of hypoglycemia may be
delayed in patients receiving anesthetics, sedatives, analgesics, β-blockers, or sympatholytics
and in those with autonomic neuropathy.
 If hypoglycemia does occur, treatment consists of administration of 50 mL of
50 %dextrose in water, which typically increases the glucose level 100 mg/dL
or 2 mg/dL/mL.

29.  Tumors of pancreatic beta cell.
 Insulinomas are rare and benign.
 Tey usually occur as an isolated fnding but may present as part of
multiple endocrine neoplasia syndrome type I (insulinoma,
hyperparathyroidism, and a pituitary tumor).

 Profound hypoglycemia can occur intraoperatively, particularly
during manipulation of the tumor; it is probably wise to include
glucose in intravenously administered fuids.

30.  Te recurrent laryngeal nerve and external
motor branch of the superior laryngeal nerve
are in intimate proximity to the gland.
 The T4/T3 ratio of secreted hormones is 10:1.
 Although only 10% of thyroid hormone
secretion is T3, T3 is three to four times more
active than T4

31.  Tyroid hormone acts directly on cardiac myocytes and vascular
smooth muscle cells.that are important for systolic contractile
function and diastolic relaxation
 Tyroid hormone increases myocardial contractility directly, decreases
systemic vascular resistance via direct vasodilation, and increases
intravascular volume.

32.  The third generation of the TSH assay
 normal level of TSH is 0.4 to 5.0 milliunits/L. A
 TSH level of 0.1 to 0.4 milliunits/L with normal levels of free
 T3 (FT3) and free T4 (FT4) is diagnostic of subclinical hyperthyroidism.
 TSH level of less than 0.03 milliunits/L with elevated T3 and T4 is diagnostic of overt
hyperthyroidism.
 TSH level of 5.0 to 10 milliunits/L with normal levels of FT3 and FT4 is diagnostic of
subclinical hypothyroidism.
 TSH level of more than 20 milliunits/L (may be as high as 200 or even 400 milliunits/L)
with reduced levels of T3 and T4 is diagnostic of overt hypothyroidism.

33.  SIGNS AND SYMPTOMS
 3 majority of cases of hyperthyroidism:
1. Graves' disease
2. toxic multinodular goiter
3. toxic adenoma.
 patient is anxious, restless, and hyperkinetic and may be emotionally unstable.
 skin is warm and moist ,the face is fushed, the hair is fine, and the nails are soft and fragile,
increased sweating and complain of heat intolerance.
 Elderly patients with unexplained cardiac failure or rhythm
disturbances— especially atrial in origin—should be evaluated for
thyrotoxicosis.

34.  exophthalmos or proptosis resulting from an infltrative
process that involves retrobulbar fat and the eyelids
 Wasting, weakness, and fatigue are common.
 tachycardia, arrhythmias and palpitations, increased myocardial
contractility and cardiac output, and cardiomegaly.

35.  occurs in 0.4% of the U.S.
 female/male ratio is 7:1
 ages of 20 and 40 years.
 Graves' disease appears to be a systemic autoimmune
 disease caused by thyroid-stimulating antibodies that bind
to TSH receptors in the thyroid
 graves:
 ophthalmopathy occurs in 30%
+dermopathy+hyperthyroidism

36. Toxic multinodular form simple goiter and
occurs mostly in patients older than 50 years of age.
 It may present with extreme thyroid enlargement that can
cause dysphagia, globus sensation, and possibly inspiratory
stridor from tracheal compression.
 mass extends into the thoracic inlet behind the sternum. In
severe cases, superior vena cava obstruction syndrome may
also be present.

37. methimazole or propylthiouracil (PTU).
PTU has the added advantage of inhibiting the peripheral conversion of
T4 to T3.
A euthyroid state achieved in 6 to 8 weeks
Side efects (3% to 12%) agranulocytosis

38.  β-Adrenergic antagonists relieve signs and symptoms such as anxiety,
sweating, heat intolerance, tremors, and tachycardia.
 Propranolol affect the peripheral conversion of T4 to T3
 surgery include hypothyroidism, hemorrhage with tracheal Complications
from compression, unilateral or bilateral damage to the recurrent laryngeal
nerve(s), damage to the motor branch of the superior laryngeal nerve, and
damage to or inadvertent removal of the parathyroid glands
 Hyperthyroidism during pregnancy is treated with low dosages of antithyroid
drugs.
 If dosages higher than 300 mg/day of PTU are needed during the frst
trimester, a subtotal thyroidectomy should be performed in the second
trimester.
 cross the placenta and can cause fetal hypothyroidism.

39. In hyperthyroid patients undergoing surgery, euthyroidism should
defnitely be established preoperatively. 6 to 8 weeks
In emergency cases ,the use of an intravenous β-blocker,
glucocorticoids ,and PTU is usually necessary.
Glucocorticoids (dexamethasone 2 mg IV every 6 hours) should be
administered to decrease hormone release and reduce the peripheral
conversion of T4 to T3.
Evaluation of the upper airway for evidence of tracheal compression
or deviation caused by a goiter is an important part of the
preoperative evaluation
Examination of chest radiographs and CT scans is ofen helpful .

40. Establishment of adequate anesthetic depth is extremely important to
avoid exaggerated sympathetic nervous system responses.
Drugs that stimulate the sympathetic nervous system (i.e., ketamine,
pancuronium, atropine, ephedrine, epinephrine)
should be avoided.
Tiopental,decreases the peripheral conversion of T4 to T3 and may have a
slight advantage over other agents for anesthesia induction.
maintenance of anesthesia, any of the potent inhalation agents may be
used.

41.  Hyperthyroid patients may have co-existing muscle disease
(e.g.myasthenia gravis) with reduced requirements for the nondepolarizing
muscle relaxants; therefore, careful titration is required.
 For the treatment of intraoperative hypotension, a direct-acting vasopressor
(phenylephrine) is preferred. Ephedrine, epinephrine, norepinephrine, and
dopamine should be avoided or administered in extremely low doses to
prevent exaggerated hemodynamic responses.
 Epinephrine containing local anesthetic solutions should be avoided.
Removal of the thyrotoxic gland does not mean immediate resolution of
thyrotoxicosis. The half-life of T4 is 7 to 8 days ;therefore, β-blocker therapy
may need to be continued in the postoperative period

42. Tyroid storm is a life-threatening exacerbation of hyperthy-
roidism precipitated by trauma, infection, medical illness, or
surgery.
Tyroid storm and malignant hyperthermia

43. The cause is probably a shift from protein-bound thyroid hormone to
free hormone as a result of the presence of circulating inhibitors to
binding.
Tyroid storm most ofen occurs in the postoperative period in
untreated or inadequately treated hyperthyroid patients afer
emergency surgery.
extreme anxiety, fever, tachycardia, cardiovascular instability, and
altered consciousness.

44. Treatment includes rapid alleviation of thyrotoxicosis and general supportive
care.
Dehydration is managed with intravenous administration of glucose-contain-ing
crystalloid solutions, and cooling measures (e.g., cooling blanket, ice packs,
administration of cool humidifed oxygen )are used to counter the fever.
β-Blockers should be titrated to decrease heart rate to less than 90 beats per
minute.
Dexamethasone 2 mg every 6 hours or cortisol 100 to 200 mg every 8 hours can be
used to decrease hormone release and conversion of T4 to T3.
Antithyroid drugs (PTU 200 to 400 mg every 8 hours) may be administered
through a nasogastric tube ,orally, or rectally.
If circulatory shock is present, intravenous administration of a direct vasopressor
(phenylephrine) is indicated.

45. SIGNS AND SYMPTOMS
0.5% to 0.8% of the adult population
most common cause in ablation of the gland by radioactive iodine or surgery. second type
idiopathic and probably autoimmune
In mild cases, patients weight gain. :fatigue ,lethargy, apathy, and listlessness. speech
becomes slow
,cold intolerance, decreased sweating, constipation, menorrhagia ,and slowing of motor
function.
cardiac output is decreased secondary to reductions in stroke volume and heart rate.
Baroreceptor function is also impaired
sinus bradycardia; ventricular dysrhythmias may also be
present.Peripheral vascular resistance is increased and blood
volume is reduced, which results in pale, cool skin.

46. Pericardial efusions are common.
Hyponatremia and impairment of free water excretion are also
common, related to inappropriate secretion of antidiuretic
hormone (ADH).
Maximum breathing capacity and difusion capacity are
decreased, and ventilatory responsiveness to hypoxia and
hypercarbia is depressed .
Pleural efusions may result in dyspnea.
adynamic ileus may occur. Deep tendon refexes demonstrate a
prolonged relaxation phase.

47. l-Tyroxine (levothyroxine sodium) is usually
administered for the treatment of hypothyroidism.

48. patients can be extremely sensitive to narcotics and sedatives and may
even be lethargic secondary to their disease; therefore, preoperative
sedation should be undertaken with caution.Airway compromise
Decreased gastric emptying increases the risk of
 regurgitation and aspiration.
 A hypodynamic cardiovascular system characterized by decreased
cardiac output, stroke volume, heart rate, baroreceptor refexes, and
intravascular volume may be compromised by surgical stress and
cardiac-depressant anesthetic agents.
 Decreased ventilatory responsiveness to hypoxia and hypercarbia is enhanced by
anesthetic agents.

49. Hypothermia occurs quickly and is difcult to treat .
Hematologic abnormalities such as anemia (25% to 50% of patients) and
dysfunction of platelets and coagulation factors especially factor VIII), electrolyte
imbalances (hyponatremia), and hypoglycemia are common and require close
monitoring intraoperatively.
Decreased neuromuscular excitability is exacerbated by anesthetic drugs.
Hypothyroid patients also appear to have an increased sensitivity to anesthetic drugs,
although the efect of thyroid activity on the minimum alveolar concentration of
volatile anesthetics is negligible.
Increased sensitivity is probably secondary to reduced cardiac output, decreased
blood volume ,abnormal baroreceptor function, decreased hepatic metabolism, and
decreased renal excretion of drugs.

50.  Hypothyroid patients are very sensitive to the myocardial-depressant efects of
the potent inhalational agents.
 Vasodilation in the presence of possible hypovolemia and impaired
baroreceptor activity can produce signifcant hypotension.
 Pharmacologic support for intraoperative hypotension is best provided with
ephedrine, dopamine, or epinephrine and not a pure α-adrenergic agonist
(phenylephrine). Unresponsive hypotension may require supplemental steroid
administration.

51.  Dextrose in normal saline is the recommended
intravenous fuid to avoid hypoglycemia and minimize
hyponatremia secondary to impaired free water
clearance.

52.  Myxedema coma is a rare severe form of hypothyroidism characterized by
delirium or unconsciousness, hypoventilation ,hypothermia (80% of
patients), bradycardia, hypotension, and a severe dilutional hyponatremia.
 It occurs most commonly in elderly women with a long history of
hypothyroidism. Infection, trauma, cold, and central nervous system
depressants predispose hypothyroid patients to myxedema coma.
 Myxedema coma is a medical emergency with a mortality rate higher
than 50% .

53.  Intravenous l-thyroxine or l-triiodothyronine is the treatment of choice.
Intravenous hydration with glucose-containing saline solutions,
temperature regulation, correction of electrolyte imbalances, and
stabilization of the cardiac and pulmonary systems are necessary.
 Mechanical ventilation is frequently required.
 Hydrocortisone 100 to 300 mg/day IV is also prescribed to treat possible
adrenal insufciency.

54.  A goiter is a swelling of the thyroid gland that results from compensatory hypertrophy and
hyperplasia of follicular epithelium secondary to a reduction in thyroid hormone output
 In most cases, a goiter is associated with a euthyroid state,
 .Surgery is indicated only if medical therapy is inefective and the goiter is compromising the airway or is
cosmetically unacceptable.
 Examination of a CT scan of the neck will demonstrate anatomic abnormalities.
 sedatives and narcotics should be avoided or used with great caution before and during endotracheal
tube placement .
 Awake intubation is the safest method to assess the degree of obstruction and establish the airway.
 Surgical removal of the mass may reveal underlying tracheomalacia and a collapsible airway.
 Tracheal extubation should be performed with as much caution and concern as intubation.

55. If the mass extends into the substernal regional (i.e., ante-
rior mediastinal mass), superior vena cava obstruction, major airway
obstruction, and/or cardiac compression may occur .
During spontaneous respiration, the larger airways are
supported by negative intrathoracic pressure, and the efects of extrinsic
compression may be apparent in only the most severe cases.
With cessation of spontaneous respiration, com-
pensatory mechanisms are removed and airway obstruction occurs. In
addition, positive pressure ventilation may demonstrate total airway
occlusion

56. A preoperative history of dyspnea in the upright or supine position
is predictive of possible airway obstruction during general
anesthesia.
A CT scan must be examined to assess the extent of the tumor
Echocardiography with the patient in the upright and supine
positions can indicate the degree of cardiac compression.
If practical, local anesthesia is recommended for patients
requiring surgery.

57.  If general anesthesia is necessary,
 In such patients, an awake intubation with fberoptic bronchoscopy using an anode tube is
 recommended. The patient is placed in semi-Fowler's position, and volatile anesthetic with
nitrous oxide and oxygen is administered using spontaneous ventilation. Muscle relaxants are
avoided.
 It must be possible to change the patient's position.
 Following tumor resection, the airway should be exam-
 ined by fberoptic bronchoscopy to detect tracheomalacia and determine whether and when
tracheal extubation is appropriate.
 A rigid bronchoscope should be available to reestablish
 the airway if collapse occurs.
 Cardiopulmonary bypass equipment should be on standby during the case.


58. Morbidity from thyroid surgery approaches 13%
Recurrent laryngeal nerve injury may be unilateral or bilateral and temporary or permanent.
Hypoparathyroidism is also a complication of thyroid surgery
The signs and symptoms of hypocalcemia occur in the frst 24 to 48 hours postoperatively. Anxiety,
circumoral numbness, tingling of the fingertips, muscle cramping, and positive Chvostek's and Trousseau's
signs are indicative of hypocalcemia.
stridor can occur and can proceed to laryngospasm.
Immediate treatment with intravenous calcium gluconate (1 g ,10 mL of a 10% solution) or calcium chloride (1
g, 10 mL of a 10% solution) is necessary.
Tracheal compression from an expanding hematoma may
cause rapid respiratory compromise in the period immediately afer thyroid surgery.
Immediate hematoma evacuation is the frst line of treatment. If time permits, the patient should
be returned to the operating room. If necessary, the wound should be opened at the bedside, clots
evacuated, and bleeding vessels secured to relieve airway obstruction.

59.  Pheochromocytomas are catecholamine-secreting
tumors that arise from chromafn cells of the
sympathoadrenal system.
Uncontrolled catecholamine release can result in
malignant hypertension, cerebrovascular accident, and
myocardial infarction.
Familial pheochromocytomas can also be part of the
MEN 2
 Most pheochromocytomas secrete norepinephrine,or
combination with a smaller amount of epinephrine

60.  the clinical presentation of pheochromocytoma is variable
 Headache, sweating, pallor, and palpitations are other classic signs
and symptoms.
 Orthostatic hypotension is also a common fnding and is considered
to be secondary to hypovolemia and impaired vasoconstrictor reflex
responses.
 Hemodynamic signs depend on the predominant catecholamine
secreted. With norepinephrine, α-adrenergic efects predominate,
and patients usually have systolic and diastolic hypertension and a
refex bradycardia.

61.  With epinephrine ,β-adrenergic efects predominate, and patients usually
have systolic hypertension, diastolic hypotension, and tachycardia.
 Cardiomyopathy is a complication of pheochromocytoma.
 Both dilated and hypertrophic cardiomyopathies, as well as lef ventricular outfow
tract obstruction, have been demonstrated echocardiographically.
 ECG abnormalities may include elevation or depression of the ST segment,
fattening or inversion of T waves, prolongation of the QT interval, high or
peaked P waves, left axis deviation, and arrhythmias.

62.  Since most pheochromocytomas secrete predominantly norepinephrine,
medical therapy has depended on α-blockade to lower blood pressure, increase
intravascular volume, prevent paroxysmal hypertensive episodes, allow
resensitization of adrenergic receptors, and decrease myocardial
dysfunction.
 Phenoxybenzamine :It is a noncompetitive α1-antagonist with some α2-
blocking properties.
 The goal of therapy is normotension, a resolution of symptoms, elimination
of ST-segment and T-wave changes on the ECG, and elimination of arrhythmias.
 Overtreatment can result in severe orthostatic hypotension.
 The optimal duration of α-blockade therapy is undetermined and may range
from 3 days to 2 weeks or longer.

63.  Because of the prolonged effect of phenoxybenzamine on α-receptors, the
recommendation has been to discontinue its use 24 to 48 hours before
surgery to avoid vascular unresponsiveness immediately following
removal of the tumor.
 Prazosin and doxazosin, pure α1-competitive blockers, are alternatives
to phenoxybenzamine. They are shorter acting, cause less tachycardia.
 A nonselective β-blocker should never be administered before α-
blockade ,because blockade of vasodilatory β2-receptors results in
unopposed α-agonism, leading to vasoconstriction and hypertensive
crises.

64. Propranolol, a nonselective β-blocker with a
half-life longer than 4 hours, is most frequently
used pheochromocytoma patients.
Esmolol has a fast onset and short elimination
half-life and can be administered intravenously
in the period immediately before surgery.
α-Methylparatyrosine (metyrosine) It is
especially useful for malignant and inoperable
tumors.

65.  Optimal prepration :α-adrenergic blocker with or
without a β-blocker with αmethylparatyrosine,
correction of hypovolemia.
 Intraoperative goals Hypertension frequently occurs
during pneumo-
 peritoneum as well as during tumor manipulation. On
the other hand, signifcant hypotension may develop
following ligation of the tumor's venous drainage.
 invasive monitoring methods

66.  transesophageal echocardiography may be necessary to manage the large fuid
requirements, major volume shifs, and possible underlying myocardial dysfunction in patients
with very active tumors.
 Factors that stimulate catecholamine release such as fear,stress, pain, shivering, hypoxia, and
hypercarbia must be minimized in the perioperative period.
 Morphine and atracurium can cause histamine release, which may provoke release of
catecholamines from the tumor. Atropine, pancuronium, and succinylcholine are examples of
vagolytic or sympathomimetic
 drugs that may stimulate the sympathetic nervous system.

67.  systolic arterial pressure in excess of 200 mm Hg Sodium
nitroprusside, a direct vasodilator, is the agent of choice
because of its potency ,immediate onset of action, and short
duration of action.
 Phentolamine, a competitive α-adrenergic blocker and a
direct vaso-dilator, is efective, although tachyphylaxis and
tachycardia are associated with its use.

68.  Nitroglycerin is efective, but large doses are ofen required and
may cause tachycardia.
 Labetalol ,with more β- than α-blocking properties, is preferred
for predominantly epinephrine-secreting tumors.
 Magnesium sulfate inhibits release of catecholamines from the
adrenal medulla and peripheral nerve terminals, reduces
sensitivity of α-receptors to catecholamines, is a direct
vasodilator, and is an antiarrhythmic.
 Increasing the depth of anesthesia is also an option
 Arrhythmias are usually ventricular in origin and are managed
with either lidocaine or β-blockers.

69.  Amiodarone, an antiarrhythmic agent that prolongs the duration of
the action potential of atrial and ventricular muscle, has been used as
an alternative to β-blockers to treat supraventricular
 tachycardia associated with hypercatecholaminemia.
 Lactated Ringer's solution and physiologic saline are the
recommended fuids for use before tumor removal.
 insulin levels increase and hypoglycemia may occur. Terefore,
dextrose-containing solutions should be added afer tumor removal.
 Glucocorticoid therapy should be administered if a bilateral
adrenalectomy is performed or if hypoadrenalism is a possibility