DM , adrenal disease, anaesthetic management,

1. Anaesthetic consideration for endocrine
diseases/ part 2
Dr. Radhwan Hazem Alkhashab
Consultant anaesthesia & ICU
2021

2. Diabetes Mellitus

3. INTRODUCTION
Diabetes mellitus is characterized by impairment of carbohydrate metabolism caused by an absolute or
relative deficiency of insulin or of insulin responsiveness, which leads to hyperglycemia and glycosuria.
Following a meal, plasma glucose increases, which stimulates an increase in plasma insulin.
Humans require insulin for survival. Diabetes mellitus results from an inadequate supply of insulin and
an inadequate tissue response to insulin, yielding increased circulating glucose levels with eventual
microvascular and macrovascular complications.

4. Types of DM
1) Type 1a diabetes is caused by an autoimmune destruction of beta cells within pancreatic
islets resulting in complete absence or barely negligible circulating insulin levels.
2) Type 1b diabetes is a rare disease with absolute insulin deficiency, although not immune
mediated.
3) Type 2 diabetes is not immune mediated and results from a relative deficiency of insulin
coupled with an insulin receptor defect or defect(s) in its postreceptor intracellular signaling
pathways.

5. Signs and Symptoms
5% to 10% of all cases of diabetes are type 1. It is usually diagnosed before the age of 40 years
and is one of the most common chronic childhood illnesses. Type 1 diabetes is caused by a
T cell–mediated autoimmune destruction of beta cells of the pancreas. At least 80% to 90%
of beta-cell function must be lost before hyperglycemia occurs. Patients demonstrate
hyperglycemia over several days to weeks associated with fatigue, weight loss, polyuria,
polydipsia, blurring of vision, and signs of intravascular volume depletion. A random blood
glucose greater than 200 mg/dL and a hemoglobin (Hb) A1c level greater than 7.0%. The
presence of ketoacidosis indicates severe insulin deficiency.
Type 1 Diabetes

6. Type 2 diabetes is responsible for 90% of all cases of
diabetes mellitus in the world. Type 2 diabetics are
typically in the middle to older age group and
overweight, although there has been a significant
increase in younger patients and even children over
the past decade. There are three important defects in
type 2 diabetes:
1) Increased rate of hepatic glucose release.
2) Impaired basal and stimulated insulin secretion,
3) Inefficient use of glucose by peripheral tissues (i.e.,
insulin resistance, which is mainly in skeletal muscle,
adipose tissue, and the liver).
Type 2 Diabetes

7. Impaired glucose tolerance is associated with an increase in
body weight, a decrease in insulin secretion, and a
reduction in peripheral insulin action. The transition to
clinical diabetes demonstrates these same factors plus an
increase in hepatic glucose production.
The metabolic syndrome or insulin-resistance syndrome is a
constellation of clinical and biochemical characteristics
frequently seen in patients with or at risk of type 2 diabetes
Metabolic Syndrome (At least three of the
following)
Fasting plasma glucose 110 mg/dL
Abdominal obesity (waist girth > 40 [in men],
35 [in women])
Serum triglycerides 150 mg/dL
Serum high-density lipoprotein cholesterol < 40 mg/dL
(men), < 50 mg/dL (women)
Blood pressure 130/85 mm Hg

8. 1.Blood glucose:
A normal fasting plasma glucose is 70 to 100 mg/dL Any
fasting glucose between 101 and 125 mg/dL is
impaired fasting glucose. Glucose levels, especially in
type 2 diabetics, usually increase over years to
decades progressing from the normal range to the
impaired glucose tolerance range and finally to
clinical diabetes.
Diagnosis
Diagnostic Criteria for Diabetes Mellitus
Symptoms of diabetes (polyuria, polydipsia, unexplained
weight loss) plus a random plasma glucose
concentration 200 mg/dL
OR
Fasting (no caloric intake for 8 hours) plasma glucose
126 mg/dL
OR
2-hour plasma glucose > 200 mg/dL during an oral
glucose tolerance test

9. 2. The Hb A1c test
HbA1C provides a valuable assessment of long-term glycemic control. Erythrocyte hemoglobin
is non enzymatically glycosylated by glucose that freely crosses red blood cell membranes.
This represent the average plasma glucose concentration during the preceding 60 to 90
days. The normal range for Hb A1c is 4% to 6%. Increased risk of microvascular and
macrovascular disease begins at a Hb A1c of 6.5%.
3. Urine glucose:
Urine glucose is a poor diagnostic test since the renal glucose threshold is not reached until the
extracellular glucose concentration exceeds 180 mg/dL.

10. Insulin is necessary to manage all type 1 diabetics and many type 2 diabetics. Conventional
insulin therapy uses twice-daily injections. Intensive insulin therapy uses three or more
daily injections or a continuous infusion.
The various forms of insulin include:-
1. Intermediate acting (NPH*, lente, lispro protamine, aspart protamine) and administered
twice daily.
2. Long acting (ultralente and glargine) and administered once daily.
3. Insulins that are short acting (regular) or rapid acting (lispro, aspart), which provide
glycemic control at mealtimes (prandial insulin).
* NPH =neutral protamine Hagedorn
Treatment of DM

11. Insulin types
Insulins Onset Peak Duration
Short Acting
1. Human regular 30 min 2-4 hr 5-8 hr
2. Lispro (Humalog) 10-15 min. 1-2 hr 3-6 hr
3. Aspart (Novolog) 10-15 min. 1-2 hr 3-6 hr
intermediate
1. Human NPH 1-2 hr 6-10 hr 10-20 hr
2. Lente 1-2 hr 6-10 hr 10-20 hr
Long acting
1. Ultralente 4-6 hr 8-20 hr 24-48 hr
2. Glargine (Lantus) 1-2 hr Peakless 24 hr

12. The cornerstones of therapy for type 2 diabetes are diet with weight loss, exercise therapy, and the
oral antidiabetic agents. Reduction of body weight through diet and exercise is the first
therapeutic measure to control type 2 diabetes. The decrease in adiposity improves hepatic and
peripheral tissue insulin sensitivity, enhances postreceptor insulin action, and may possibly
increase insulin secretion.
Oral Antidiabetic Agents
The four major classes of oral agents are:-
1) Secretagogues (sulfonylureas, meglitinides), which stimulate insulin secretion from pancreatic
beta cells.
2) Biguanides (metformin), which suppress excessive hepatic glucose release.
3) Thiazolidinediones or glitazones (rosiglitazone, pioglitazone), which improve insulin sensitivity.
4) a-glucosidase inhibitors (acarbose, miglitol), which delay gastrointestinal glucose absorption.
Treatment…cont.

13. These agents, either as monotherapy or
in various combinations, are used to
maintain glucose control (fasting
glucose, 90–130 mg/dL; peak
postprandial glucose, <180 mg/dL,
Hb A1c <7%) in the initial stages of
the disease.

14. Sulphonylureas are a class of oral (tablet) medications that control blood sugar levels in patients with type 2
diabetes by stimulating the production of insulin in the pancreas and increasing the effectiveness of
insulin in the body.
They are generally taken once or twice a day, with or shortly before a meal, and can be taken on their own or
prescribed for use alongside other diabetes drugs such as metformin
Drugs in this class
The following drugs are all in the sulphonylureas class (trade name first, generic name in brackets):
Amaryl (Glimepiride)
Daonil (Gilbenclamide)
Glibenese (Glipizide)
Tolbutamide (Tolbutamide).
.
Sulphonylureas

15. Theses groups of drugs which decrease hepatic gluconeogenesis and to a lesser degree
enhance utilization of glucose by skeletal muscle and adipose tissue by increasing glucose
transport across cell membranes. In addition to lowering glucose levels, they decrease
plasma triglycerides and low-density lipoprotein cholesterol levels and reduce postprandial
hyperlipemia and plasma free fatty acid levels and their oxidation.
The biguanides

16. Thiazolidinediones, also known as glitazones, are a group of oral anti-diabetic drugs designed to
treat patients with type 2 diabetes. Classed as oral hypoglycemic drugs, they are taken once
or twice daily with or without food and work by targeting insulin resistance – a core
physiologic defect in those with type 2 diabetes.
Thiazolidinediones

17. These drugs block the breakdown of starchy foods such as bread, potatoes, and pasta, and they
slow down the absorption of some sugars, such as table sugar. You take an alpha-
glucosidase inhibitor with the first bite of each meal. Most people take a pill three times a day.
α-glucosidase inhibitors

18. Complications of DM

19. Diabetic ketoacidosis (DKA) is a complication of decompensated diabetes mellitus. The signs and
symptoms of DKA are primarily the result of abnormalities in carbohydrate and fat metabolism.
Episodes of DKA occur more commonly in type 1 diabetics and are precipitated by infection or
acute illness (cerebrovascular accident, myocardial infarction, acute pancreatitis).
High glucose levels exceed the threshold for renal tubular absorption creating a significant
osmotic diuresis with marked hypovolemia. A tight metabolic coupling between hepatic
gluconeogenesis and ketogenesis results in an overproduction of ketoacids by the liver. An
increase in ketoacid (b-hydroxybutyrate, acetoacetate, acetone) production creates a metabolic
acidosis. An increased anion gap (Na-[ Cl+HCO3 ]) normal: (8-14 mEq/L) is present.
Substantial deficits of water, potassium, and phosphorus exist, although laboratory values of
these electrolytes appear normal or elevated. Hyponatremia results from the effect of
hyperglycemia and hyperosmolarity on water distribution.
1. Diabetic ketoacidosis

20. Diagnostic Features of DKA

21. The treatment of DKA consists of giving large amounts of normal saline, effective doses of
insulin, and electrolyte supplementation. Rehydration alone will reduce plasma glucose
levels by 30% to 50% and possibly more. An intravenous loading dose of 0.1 U/kg of
regular insulin plus a low-dose insulin infusion of 0.1 U/kg per hour is initiated. The
average decline in blood glucose is 75 to 100 mg/dL per hour with correction to target
values ( 250 mg/dL) occurring in 4 to 6 hours and correction to target values for acidosis
and HCO3 levels in 8 to 12 hours. A normal pH is obtained in approximately 24 hours.
Insulin administration is necessary until a normal acid base status is achieved.
Treatment of DKA

22. Magnesium is replaced as needed. Sodium bicarbonate is administered for a pH less than 7.1.
The infrequent but devastating development of cerebral edema results from correction of
hyperglycemia without simultaneous elevation of plasma Na. The overall mortality rate for
DKA is 5% to 10% and 15% to 28% for patients older than 65 years of age and may approach
45% in patients with coma
DKA… cont.

23. Hyperglycemic hyperosmolar syndrome (HHS) is characterized by severe hyperglycemia, hyperosmolarity,
and dehydration usually in elderly (older than 60 years) type 2 diabetics.
Predisposing factors:Acute illness such as
1. Infection.
2. Myocardial infarction.
3. Cerebrovascular accident.
4. Pancreatitis.
5. Intestinal obstruction.
6. Endocrinopathy.
7. Renal failure.
8. Burn.
2. Hyperglycemic hyperosmolar syndrome (HHS)

24. The patient presents with polyuria, polydipsia, hypovolemia, hypotension, tachycardia, and organ
hypoperfusion.
The early administration of large volumes of crystalloid fluids is necessary to prevent this
syndrome. Hyperosmolarity (>340 mOsm/L) is responsible for an obtunded mental status or
coma
Patients may have some degree of metabolic acidosis but do not demonstrate a ketosis. Vascular
occlusions secondary to mesenteric artery thrombosis, or diffuse intravascular coagulation are
an important complication of HHS.
S. & S. of HHS

25. Treatment includes significant fluid resuscitation, insulin, and electrolyte supplementation. If
the plasma osmolarity* is greater than 320 mOsm/L, large volumes (1000–1500 mL/hr) of
0.45% normal saline should be administered until the osmolarity is less than 320 mOsm/L,
at which time large volumes (1000–1500 mL/hr) of 0.9% normal saline is administered.
Insulin is initiated with an intravenous bolus of 15 units of regular insulin followed by a 0.1-
U/kg per hour infusion. The insulin infusion is decreased to 2 to 3 U/ hr when the glucose
decreases to 250 to 300 mg/Dl.
The mortality rate of HHS is 10% to 15%.
*Osmolarity =2 (Na+) + 2 (K+) + Glucose + Urea (all in mmol/L)
Treatment of HHS

26. HHS
DKA

27. 1. Nephropathy
Approximately 30% to 40% of type 1 diabetics and 5% to 10% of type 2 diabetics develop end-
stage renal disease. The kidneys demonstrate glomerulosclerosis with glomerular
basement membrane thickening, arteriosclerosis, and tubulointerstitial disease. The
clinical course is characterized by hypertension, albuminuria, peripheral edema,
and a progressive decrease in glomerular filtration rate. Basement membrane thickening
develops within 2 to 3 years of the diagnosis of diabetes. Renal function remains normal
on laboratory testing for approximately 15 years, at which time proteinuria develops,
indicating advanced glomerulosclerosis. Proteinuria is the earliest laboratory manifestation
of diabetic renal disease. Within 5 years of proteinuria, the blood urea nitrogen and
creatinine increase and a significant percentage of these patients progress to renal failure
in 3 to 5 years.
3. Microvascular Complications

28. Treatment of hypertension can markedly slow progression. Hypertension is managed with a low-
sodium diet, low doses of diuretics, and one or several antihypertensive agents including a
b1-antagonist, ACE inhibitor, angiotensin II receptor blocker, calcium channel blocker, and/or
an a1-blocker.
Even though b-blockers can cause hypoglycemia by inhibiting hepatic glucose production, and
masking the clinical signs of hypoglycemia, they are still highly effective. ACE inhibitors
provide an added benefit in diabetics by retarding the progression of proteinuria and the
decrease in the glomerular filtration rate.
If end-stage renal disease develops, there are four options: hemodialysis, peritoneal dialysis,
continuous ambulatory peritoneal dialysis, and transplantation.
Treatment of nephropathy

29. 2. Peripheral Neuropathy
More than 50% of patients who have had diabetes for more than 25 years will develop a peripheral
neuropathy.
3. Retinopathy
Diabetic retinopathy results from a variety of microvascular changes including occlusion, dilation,
increased permeability, and microaneurysm formation resulting in hemorrhages, exudates,
and growth of abnormal vessels and fibrous tissue. Visual impairment can range from minor
changes in color vision to total blindness. Strict glycemic control and blood pressure control
can reduce the risk of development and progression of retinopathy

30.  Cardiovascular disease
Is a major cause of morbidity and the leading cause of mortality in diabetics. It commonly
presents as angina, a myocardial infarction, congestive heart failure, or sudden death and
results from atherosclerotic coronary artery disease and hypertension. A dyslipidemia is the
major contributor to the initiation and development of atherosclerotic lesions.
Statin therapy should be considered for all diabetics.
Medical management of symptomatic coronary artery disease includes b1-blockers, ACE
inhibitors, nitrates, calcium channel blockers, statins, fibrates, antiplatelet drugs, and
possibly thrombolysis, stent placements, or, in severe cases, coronary artery bypass.
4. Macrovascular Complications

31.  Diabetic autonomic neuropathy (DAN) : can affect any part of the autonomic nervous
system,
 Cardiovascular autonomic neuropathy is a common type of DAN and is characterized by
abnormalities in heart rate control and central/peripheral vascular dynamics. A resting tachycardia
and a loss of heart rate variability during deep breathing are early signs. The heart may
demonstrate systolic and diastolic dysfunction with a reduced ejection fraction. Dysrhythmias may
be responsible for an episode of sudden death. Patients with coronary artery disease may be
asymptomatic during ischemic events.
 Respiratory DAN: Impaired respiratory reflexes and impaired ventilatory responses to hypoxia and
hypercapnia.
 Gastrointestinal DAN : cause impair gastric secretion and gastric motility, causing gastroparesis,
nausea, vomiting, early satiety, bloating, and epigastric pain. Treatment of gastroparesis includes
strict blood glucose control, multiple small meals, reduced fat content in meals, and prokinetic
agents such as metoclopramide.
Diarrhea and constipation are also common among diabetics and may be related to DAN.

32. The stress response of surgery creates the classic hyperglycemic challenge. Activation of the
sympathetic nervous system and release of catecholamines, cortisol, and growth hormone
may be sufficient to convert a well-controlled diabetic to one with significant hyperglycemia
and even ketoacidosis. In addition, surgery is associated with a reduction in insulin
sensitivity (insulin resistance of surgery) in the periphery.
Acute hyperglycemia causes dehydration, impaired wound healing, an increased rate of infection,
worsening central nervous system/spinal cord injury with ischemia, and hyperviscosity with
thrombogenesis.
Management of Anesthesia

33. B1-Antagonists should be used if coronary artery disease is present to decrease morbidity and
mortality perioperatively. For renal disease, control of hypertension is a major priority,
using ACE inhibitors. The presence of an autonomic neuropathy predisposes the patient to
perioperative dysrhythmias and intraoperative hypotension, gastroparesis with possible
aspiration, and hypoglycemia unawareness. Preoperative evaluation of the musculoskeletal
system should focus on limited joint mobility of the neck
Preoperative preparations

34. Management of insulin in the preoperative period depends on the type of insulin that the
patient takes and the timing of dosing. 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. A 5% dextrose with 0.45% normal saline (D5 1=2 NS) intravenous infusion at 100
mL/hr should be initiated preoperatively. Oral hypoglycemics should be discontinued 24 to
48 hours preoperatively.
The sulfonylureas should also be avoided during the entire perioperative period since they
block myocardial potassium adenosine triphosphate channels, which are responsible for
ischemia.
(*NPH =neutral protamine Hagedorn)

35. Well-controlled type 2 diabetics do not require insulin for minor surgery. Poorly controlled type 2
diabetics and all type 1 diabetics having minor surgery and all diabetics having major surgery
need insulin. For major surgery, if the serum glucose is greater than 270 mg/dL
preoperatively, the surgery should be delayed while rapid control is achieved with
intravenous insulin. If the serum glucose is greater than 400 mg/dL, the surgery should be
postponed and the metabolic state restabilized

36. The goal of intraoperative blood glucose management is to avoid hypoglycemia while maintaining
blood glucose below 180 mg/dL.
There are several common perioperative management regimens for insulin-dependent diabetic
patients. The patient receives a fraction—usually half—of the total morning insulin dose in the
form of intermediate-acting insulin To decrease the risk of hypoglycemia, insulin is
administered after intravenous access has been established and the morning blood glucose
level is checked. For example, a patient who normally takes 30 units of NPH (neutral protamine
Hagedorn; intermediate-acting) insulin and 10 units of regular or Lispro (short-acting) insulin or
insulin analogue each morning and whose blood glucose is at least 150 mg/dL would receive
15 units (half the normal 30-unit morning dose) of NPH subcutaneously before surgery along
with an infusion of 5% dextrose solution (1.5 mL/kg/h).
Intraoperative management

37. Absorption of subcutaneous or intramuscular insulin depends on tissue blood flow, however,
and can be unpredictable during surgery.
Supplemental dextrose can be administered if the patient becomes hypoglycemic (<100
mg/dL). However, intraoperative hyperglycemia (>150–180 mg/dL) is treated with
intravenous regular insulin according to a sliding scale. One unit of regular insulin given to
an adult usually lowers plasma glucose by 25–30 mg/dL.
An alternative method is to administer regular insulin as a continuous infusion. Regular insulin
can be added to normal saline in a concentration of 1 unit/mL and the infusion begun at 0.1
unit/kg/h.
A general target for the intraoperative maintenance of blood glucose is less than 180
mg/dL.

38. When administering an intravenous insulin infusion to surgical patients, adding some (eg, 20 mEq)
KCl to each liter of fluid may be useful, as insulin causes an intracellular potassium shift.
If the patient is taking an oral hypoglycemic agent preoperatively, the drug can be continued until
the day of surgery. However, sulfonylureas and metformin have long half lives and many
clinicians will discontinue them 24–48 h before surgery. They can be started postoperatively
when the patient resumes oral intake.
The effects of oral hypoglycemic drugs with a short duration of action can be prolonged in the
presence of kidney failure.

39. Sliding scale insulin

40. Aggressive insulin therapy in the intensive care unit (ICU) has demonstrated significant
benefit in morbidity and mortality.
Postoperative

41. Emergency surgery places diabetics at risk of developing DKA or HHS. Surgery should be
delayed for 4 to 6 hours to optimize the patient’s metabolic status. DKA is more likely to
develop in type 1 diabetics and is usually precipitated by infection, gastrointestinal
obstruction, or trauma in the surgical patient. Total body deficits of sodium and potassium
are present, and frequently phosphate and magnesium deficits exist. Treatment includes
large volumes of normal saline and insulin. An insulin bolus of 0.1 U/kg followed by an
infusion of 0.1 U/kg per hour is the initial prescription. Serum glucose is monitored hourly,
and electrolytes are monitored every 2 hours.
Potassium, magnesium, and phosphate deficits are replaced when urine production is
documented. When serum glucose decreases to less than 250 mg/dL, intravenous fluids
should include dextrose. Insulin is continued until acidosis resolves. Sodium bicarbonate is
not routinely given and is reserved for cases where the pH is less than 7.10.
Emergency Surgery

42. Adrenal glands

43. The adrenal glands consist of the adrenal cortex and the adrenal medulla. The adrenal cortex is
responsible for the synthesis of three groups of hormones classified as glucocorticoids,
mineralocorticoids (aldosterone), and androgens.
Introduction

44. Cushing’s syndrome is categorized as
1) ACTH-dependent Cushing’s syndrome (inappropriately high plasma ACTH concentrations
stimulate the adrenal cortex to produce excessive amounts of cortisol).
2) ACTH-independent Cushing’s syndrome (excessive production of cortisol by abnormal
adrenocortical tissues causes the syndrome and suppresses secretion of CRH and ACTH).
Hypercortisolism (Cushing’s Syndrome)

45. Clinical diagnosis:
1) sudden onset of weight gain, which is usually central
2) Thickening of the facial fat, which rounds the facial contour (moon facies).
3) Systemic hypertension.
4) Glucose intolerance.
5) Oligomenorrhea or amenorrhea in premenopausal women.
6) Spontaneous ecchymoses.
7) Skeletal muscle wasting and weakness manifest as difficulty climbing stairs.
8) Depression and insomnia.
Laboratory diagnosis:
The diagnosis of Cushing’s syndrome is confirmed by demonstrating cortisol hypersecretion
based on 24-hour urinary secretion of cortisol.
Diagnosis

46. The treatment of choice for patients with Cushing’s disease is transsphenoidal
microadenomectomy. Alternatively, patients may undergo 85% to 90% resection of the
anterior pituitary. Pituitary radiation and bilateral total adrenalectomy are necessary in some
patients. Surgical removal of the adrenal gland is the treatment for adrenal adenoma or
carcinoma.
Treatment

47. Preoperative evaluation of systemic blood pressure, electrolyte balance, and the blood glucose
concentration are especially important. Osteoporosis is a consideration when positioning
patients for the operative procedure. Etomidate may transiently decrease the synthesis and
release of cortisol by the adrenal cortex. Attempts to decrease adrenal cortex activity with
opioids, barbiturates, or volatile anesthetics are probably futile, as any drug-induced
inhibition is likely overridden by surgical stimulation. Even regional anesthesia may not be
effective in preventing increased cortisol secretion during surgery.
Management of Anesthesia

48. Doses of muscle relaxants should probably be decreased initially in view of skeletal muscle
weakness, which frequently accompanies hypercortisolism. In addition, the presence of
hypokalemia could influence responses to non depolarizing muscle relaxants.
Plasma cortisol concentrations decrease promptly after microadenomectomy or bilateral
adrenalectomy, for which replacement therapy is recommended. In this regard, a continuous
infusion of cortisol (100 mg/day IV) may be initiated intraoperatively.

49. Primary hyperaldosteronism (Conn’s syndrome) is present when there is excess secretion of
aldosterone from a functional tumor (aldosteronoma.). Occasionally, primary aldosteronism is
associated with pheochromocytoma, primary hyperparathyroidism, or acromegaly. Secondary
hyperaldosteronism is present when increased circulating serum concentrations of renin, as
associated with renovascular hypertension, stimulate the release of aldosterone.
Hyperaldosteronism (Conn’s syndrome)

50. Symptoms may reflect systemic hypertension (headache) or hypokalemia (polyuria, nocturia,
skeletal muscle cramps, skeletal muscle weakness). Systemic hypertension (diastolic blood
pressure often 100–125 mm Hg) reflects aldosterone-induced sodium retention and the
resulting increased extracellular fluid volume. This hypertension may be resistant to treatment.
Aldosterone promotes renal excretion of potassium resulting in hypokalemic metabolic
alkalosis. Skeletal muscle weakness is presumed to reflect hypokalemia. Hypomagnesemia
and abnormal glucose tolerance may be present.
Signs & symptoms

51. Diagnosis
Spontaneous hypokalemia in patients with systemic hypertension is highly suggestive of
aldosteronism. Plasma renin activity is suppressed in almost all patients with untreated
primary aldosteronism and in many with essential hypertension; with secondary
aldosteronism, however, the plasma renin activity is high.
Treatment
Initial treatment of hyperaldosteronism consists of supplemental potassium and
administration of a competitive aldosterone antagonist, such as spironolactone. Systemic
hypertension may require treatment with antihypertensive drugs.
Definitive treatment for an aldosterone-secreting tumor is surgical excision. Bilateral
adrenalectomy may be necessary if multiple aldosterone-secreting tumors are found.

52. Management of anesthesia for the treatment of hyperaldosteronism is facilitated by
preoperative correction of hypokalemia and treatment of systemic hypertension.
Persistence of hypokalemia may modify responses to non depolarizing muscle relaxants.
Furthermore, it must be appreciated that intraoperative hyperventilation of the patient’s
lungs can decrease the plasma potassium concentration. Inhaled or injected drugs are
acceptable for maintenance of anesthesia. Measurement of cardiac filling pressures via a
right atrial or pulmonary artery catheter may be useful during surgery for adequate
evaluation of the intravascular fluid volume and the response to intravenous infusion of
fluids.
Management of Anesthesia

53. Indeed, aggressive preoperative preparation can convert the excessive intravascular fluid volume
status of these patients to unexpected hypovolemia, manifesting as hypotension in response to
vasodilating anesthetic drugs, positive pressure ventilation of the lungs, body position changes,
or sudden surgical blood loss.
Acid base status and plasma electrolyte concentrations should be measured frequently during the
perioperative period. A continuous intravenous infusion of cortisol, 100 mg every 24 hours, may
be initiated on an empirical basis if transient hypocortisolism due to surgical manipulation is a
consideration.

54. Adrenal Insufficiency

55. There are two types of AI:
1) Primary disease (Addison’s disease), the adrenal glands are unable to elaborate sufficient
quantities of glucocorticoid, mineralocorticoid, and androgen hormones. The most common
etiology for this rare endocrinopathy is bilateral adrenal destruction from autoimmune
disease. fatigue, weakness, anorexia, nausea and vomiting, cutaneous and mucosal
hyperpigmentation, hypovolemia, hyponatremia, and hyperkalemia.
2) Secondary AI, a failure in elaboration of CRH or ACTH occurs secondary to
hypothalamic/pituitary disease or suppression of the hypothalamic-pituitary axis. Unlike
Addison’s disease, there is only a glucocorticoid deficiency with secondary disease. The
most common cause is iatrogenic and includes pituitary surgery, pituitary irradiation, or
most commonly the use of synthetic glucocorticoids.
Signs and Symptoms

56. Cortisol accounts for 95% of the adrenal gland’s glucocorticoid activity, with corticosterone and
cortisone contributing some activity. Estimates of daily cortisol secretion are the equivalent
of 15 to 25 mg/day of hydrocortisone.
Surgery is one of the most potent and best studied activators of the hypothalamic-pituitary-
adrenal (HPA) axis. The degree of activation of the axis depends on the magnitude and
duration of surgery and the type and depth of anesthesia. During surgery in patients with an
intact normally functioning HPA axis, CRH, ACTH, and cortisol levels all increase
significantly. Deep general anesthesia or regional anesthesia postpones the usual
intraoperative glucocorticoid surge until the postoperative period. Increases in ACTH begin
with surgical incision and remain elevated during surgery with the peak level occurring with
pharmacologic reversal of muscle relaxants and extubation of the patient at the end of the
procedure and continuing into the immediate postoperative period.

57. During major surgery, cortisol release may increase from a preoperative level of 15 to 25 mg/day
to 75 to 150 mg/day, yielding a plasma cortisol level of 30 to 50 mg/dL. An uncomplicated
cholecystectomy in an otherwise normal patient will yield a plasma cortisol level of 27 to 34
mg/dL 30 minutes after incision and 46 to 49 mg/dL 5 hours after surgery. Patients in the
ICU may demonstrate plasma cortisol levels greater than 60 mg/dL.

58. Diagnosis
Critically ill patients with cortisol levels less than 20 mg/Dl have AI. The classic definition of
AI includes a baseline plasma cortisol less than 20 mg/dL and a cortisol level less than 20
mg/dL following an ACTH stimulation test.
Treatment
Patients take steroid preparations to treat a number of illnesses, Those who take steroids long
term may exhibit signs and symptoms of AI during the stressful perioperative period. This
presentation may be secondary to prolonged hypothalamic/pituitary suppression and/or
inadequate exogenous steroid replacement. In addition, if steroids are abruptly withdrawn in
the perioperative period, the manifestations of AI may appear within 24 to 36 hours. For
patients with a history of long-term steroid use, it may take 6 to 12 months from the time of
discontinuation of the steroids for the adrenal glands to recover full function.

59. Patients taking prednisone less than 5 mg/day (morning dose) for any length of time, even years,
do not demonstrate clinically significant HPA axis suppression and do not require
perioperative supplementation, although they need to receive their normal daily steroid dose.
Any patient who has received a glucocorticoid in doses equivalent to more than 20 mg/day
of prednisone for more than 3 weeks within the past year is considered to have adrenal
suppression and is at risk of AI and needs perioperative supplementation. Patients receiving
more than 2 g/day of topical steroids or more than 0.8 mg/day of inhaled steroids on a long-
term basis may have adrenal suppression and should probably receive supplementation.

60. No specific anesthetic agent(s) and/or technique(s) are recommended in managing patients
with or at risk of AI. Etomidate inhibits the synthesis of cortisol transiently in normal
patients and should be avoided in this patient population. Patients with untreated AI
presenting for emergency surgery should be managed aggressively with invasive monitoring
including an arterial catheter and a central venous or pulmonary artery catheter, intravenous
corticosteroids, and fluid and electrolyte resuscitation.
Management of Anesthesia of AI