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40. What syndromes are associated with a pheochromocytoma?
Various syndromes can be associated with a pheochromocytoma; thus, once diagnosed, a further
work-up may be necessary. If one of the syndromes is diagnosed, the possibility of a pheochromocytoma may need to be explored.
Possible associated syndromes are neurofibromatosis, MEN 2a, MEN 2b, von Hippel-Lindau
syndrome, and para-glanduloma syndromes.
41. What is multiple endocrine neoplasia (MEN) syndrome?
This is a syndrome by which at least two hormone-producing organs or tissues contain neoplasms.
These findings are usually associated with several members of the same family.
42. What are the different types of MEN?
MEN 1 (Wermer’s syndrome) is the most common MEN syndrome characterized by tumors of the
parathyroid, pituitary, and pancreas.
MEN 2a is characterized by medullary thyroid carcinoma, hyperparathyroidism, and
pheochromocytoma.
MEN 2b is characterized by medullary thyroid carcinoma, pheochromocytoma, and mucosal
neuromas.
Treatment in general for all types of MEN can be complicated and requires a team approach.
The modalities of treatment usually are strategically planned surgery and medial management of the
various hormonal imbalances and consequences.
43. What is diabetes insipidus?
Diabetes insipidus is characterized by a decrease in ADH (vasopressin), causing a decreased ability to
concentrate urine at the renal tubules, therefore leading to excessive water loss. This results in a large
amount of excreted dilute urine.
The three potential sites of alteration in ADH are the pituitary, the neurohypophysis, and the
kidney.
The symptoms of diabetes insipidus are polyuria and polydipsia, which mimic some symptoms of
diabetes mellitus. It is important not to confuse the two disease entities.
44. What are the two types of diabetes insipidus (DI)?
1. Central DI is a decrease in the production of ADH, which can be caused by some of the following:
head trauma, tumors, surgery, autoimmune disorders, and Langerhans histiocytosis X.
2. Nephrogenic DI is a decrease in the kidney response to circulating ADH, which can be caused by
chronic renal disease and sickle cell anemia.
45. How is DI diagnosed?
DI is characterized by diluted urine with increased serum osmolality. The diagnosis is made by fluid
restriction for 6 to 10 hours. A patient with an intact neurohypophyseal axis will increase urine osmolality up to 500 to 1400 mEq/L while keeping serum osmolality <295 mEq/L. A patient with full-blown
DI cannot protect his or her serum osmolality. As a result, levels of serum osmolality >320 with a urine
osmolality <200 may be seen. When this patient is given parenteral ADH, the urine osmolality rises
significantly.
46. How is central DI treated?
Treatment for central DI depends on etiology. DI due to trauma or surgery is often transient and self-
limited. DDAVP (1-deamino-8-d-arginine vasopressin), an ADH analogue with an antidiuretic pressor
activity ratio of 2000:1, is the treatment of choice for DI from other etiologies. Duration of action is 6
to 20 hours when taken intranasally or subcutaneously. It requires once- or twice-daily dosing.
MANAGEMENT CONSIDERATIONS TO THE PREGNANT PATIENT
47. What is the normal human gestation time?
Pregnancy lasts approximately 275 days, or 40 weeks divided into trimesters.
48. A 22-week pregnant woman is in which trimester?
She is in her second trimester. The trimester system is:
• Firsttrimester(0to14weeks)
• Secondtrimester(14to27weeks)
• Thirdtrimester(28to40weeks)
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49. What are the development milestones for a normally developing fetus?
• 24weeks:Lowendoffetalsurvival
• 34weeks:Lungmaturation;fetalsurvivalincreasesexponentially.Mortalityisequalto37weeks;
however, there is a much higher morbidity. Common fetal complications include feeding and temperature control issues, as well as an increased risk of neonatal jaundice.
• 37weeks:Fetalmortalitysameasat40weeks;thereforethisisconsideredatermpregnancy.
• 39weeks:Fetalmorbidityissolowastopermitelectivedelivery.
50. When does organogenesis take place?
Weeks 3 to 14.
• Weeks1to2:Embryoimplantations—allornoresponsetoembryoinsult
• Weeks3to14:Organogenesis—extremelysensitivetoexogenousinsults
• Weeks14to27:Fetuslesssensitivetoexogenousinsult.Fetalheartsoundcanbeheardforfirsttime.
• Weeks28to40:Fetusbecomessensitivetotransplacentalcarcinogens.
51. What are the FDA categories for pregnant and lactating patients?
A: Controlled studies in humans have failed to demonstrate a risk to the fetus, and the possibility of
fetal harm seems remote.
B: Animal studies have not indicated fetal risk, and there are no human studies; or animal studies
have shown a risk, but controlled human studies have not.
C: Animal studies have shown a risk, but there are no controlled human studies; or no studies are
available in humans or animals.
D: Evidence of human fetal risk exists, but in certain situations, the drug may be used despite its risk.
X: Evidence of fetal abnormalities or fetal risk based on human experience exists. The risk outweighs
any possible benefit for use during pregnancy.
52. What are the FDA drug classes for antibiotics commonly used by oral and
maxillofacial surgeons (OMFS)?
Class B: penicillin, erythromycin, clindamycin, cephalosporins, metronidazole
Class D: tetracycline, quinolones
53. What are the FDA drug classes for analgesics?
Class B:
• Acetaminophen
• Ibuprofen(Itcanbegiveninfirst32weeks;pastthat,theoreticalriskofprematureclosureofthe
patent ductus arteriosus [PDA]. This is true of all nonsteroidal antiinflammatory drugs [NSAIDs].)
• Oxycodone
• Morphine
• Fentanyl
• Meperidine
• Hydrocodone
There is concern for fetal dependence with any opioid, as well as respiratory depression in the
newborn recently exposed to opioids.
Class C:
• Codeine:associatedwithfirsttrimestermalformations;canuseinsecondorthirdtrimester
• Aspirin:associatedwithlate-termintrauterinegrowthrestriction
54. What are the FDA drug classes for common sedatives used in OMFS?
Both benzodiazepines and barbiturates pose a risk for fetal craniofacial anomalies and are FDA Class D drugs.
55. What are the FDA drug classes for common local anesthetics used in OMFS?
Category B Category C
Lidocaine Articaine
Prilocaine Bupivacaine
Etidocaine Mepivacaine
56. What is the effect of pregnancy on the cardiovascular system?
The physiologic state of pregnancy increases demand on the cardiovascular system. Gravid women
have a need for increased blood volume and increased cardiac output to allow for additional blood
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supply needed for fetal perfusion. This increase in volume can lead to a dilutional anemia and possibly
an extra heart sound (S3 or systolic murmur).
Fetal size and uterine position can also lead to aortocaval compression especially in the supine
position, therefore increasing pressure and decreasing venous return.
57. How is the respiratory system compromised with pregnancy?
The gravid patient will have an increase in O2 demand and O2 consumption. These patients also
exhibit a decrease in functional residual capacity, a low PCO2, thus resulting in an increased in minute
ventilation.
58. What is the hypercoagulable state of pregnancy?
Pregnancy has a global effect on the gravid woman, leading to an increase in thrombin, coagulation
factors, and hemoglobin. The other important change is a mechanical compression of the venous
system from the uterus, causing venous stasis. This combination ultimately leads to an increased risk
of deep venous thrombosis (DVT) and pulmonary embolus (PE).
59. How do you treat a gravid woman with a DVT?
The usual treatment of a DVT is the administration of heparin. Heparin is preferred over Coumadin for
treatment due to the fact that heparin does not cross the placenta due to its increased molecular size.
The fear of fetal toxicity with Coumadin is always a concern. There is no good data to show which form
of heparin is more advantageous—either low molecular weight heparin or unfractionated heparin.
60. Which clotting factors are altered during pregnancy?
Factors XI and XII are increased during pregnancy.
61. What are the elements of Virchow’s triad?
A hypercoagulable state, venous stasis, and endothelial wall damage.
62. Can pregnant women demonstrate a physiologic leukocytosis?
In the pregnancy state, there is an increase in cortisol and release of catecholamines that can lead to
an increase in circulating white blood cells due to demarginaton of the endothelium.
63. When is the best time to treat a pregnant woman surgically?
The second trimester is the best time for treatment; however it is still suggested to wait until the
woman is postpartum for elective procedures.
64. Why is GERD a common symptom in pregnancy?
There is little evidence to support any change in gastric volume or pH during pregnancy. However,
gastroesophageal sphincter tone is decreased leading to GERD. The actual reason for a decrease in
sphincter tone is unclear, as no underlying causality is agreed upon in the literature.
65. Is kidney function altered during pregnancy?
The gravid woman has an increase in blood volume and an increase in cardiac output, and therefore
an increase in renal plasma flow. This ultimately causes an increase in glomerular filtration rate (GFR).
This increase in GFR can lead to increased clearance of creatinine and urea.
66. Why is local anesthesia administration with epinephrine a concern in a pregnant
patient?
Local anesthetic is often prepared with a vasoconstrictor, such as epinephrine, to increase the longev-
ity and effectiveness of the anesthetic. The concern in pregnancy is the risk of uterine artery constriction, thus decreasing fetal blood flow, if the epinephrine is injected intravascular.
67. What are the potential effects of nitrous oxide during pregnancy?
Animal models have shown that nitrous oxide will have an effect on uterine blood flow by vasocon-
striction and increasing the androgenic tone of the uterus. The consequences of this physiologic action
are abortion and congenital anomalies.
68. What are the major concerns of general anesthesia during pregnancy?
It is acceptable to have general anesthesia during pregnancy as long as the preoperative and intraop-
erative management are understood and followed closely.
The major concerns are hypoglycemia, hypotension, hypothermia, and hypoxia. If these factors
are controlled, there is no data that supports a risk of fetal anomalies, miscarriage, or preterm labor
during surgery.
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69. Do antibiotics have an effect on the fetus in utero?
Most antibiotics are acceptable during pregnancy; however some antibiotics are not considered safe
during pregnancy. Sulfonamides given late in gestation can cause hyperbilirubinemia and kernicterus.
Tetracycline given after the fifth month of gestation can stain the bone. Chloramphenicol can produce
neonatal toxicity. Amino glycosides can cause fetal ototoxicity and nephrotoxicity. Fluoroquinolones
can carry risk of arthropathy.
70. Why is it recommended to restrict the use of NSAIDS during pregnancy?
The restriction of NSAIDS is recommended to prevent premature closure of the fetal ductus arteriosus,
which is necessary for fetal circulation. Other possible concerns in the last trimester with the use of
ibuprofen are low amniotic fluid and inhibition of labor.
71. Why are benzodiazepines not recommended during pregnancy?
Benzodiazepines are considered to be teratogenic.
72. Can a gravid woman be prescribed narcotics?
Narcotics given for a short period of time are considered safe for the fetus even though they cross the
placenta.
73. Why should the supine position be avoided when treating a gravid woman?
Placing a pregnant woman in the supine position will increase the pressure on the aorta and
vena cava by the gravid uterus. This position will increase blood pressure and decrease venous
return.
74. What is placental abruption?
Abruption is a traumatic separation of the placenta from the uterine wall, resulting in uncontrollable
bleeding. This state of excessive bleeding can lead to preterm delivery, fetal death, DIC, and possible
maternal death.
75. What are the clinical hallmarks of abruption?
The typical hallmarks of abruption are vaginal bleeding, uterine bleeding that leads to uterine
hypertonicity, and fetal distress.
76. Is general anesthesia safe in the pregnant patient?
If possible, it is best to treat a pregnant patient in the second trimester. In the preoperative stage,
the practitioner should consider aspiration prophylaxis with antacid or h2 antagonist. During intubation it is important to remember the pregnant patient’s airway is more edematous and vascular,
which may lead to bleeding or could decrease the view of the cords. Intra-operatively, it is important to control fluid administration, blood pressure control, and good oxygenation. If possible, fetal
monitoring is recommended. There is no evidence as to what anesthetic is best for the pregnant
patient.
77. What is the benefit of regional anesthetic techniques versus general anesthesia?
Regional anesthetics have the advantage of decreasing fetal exposure of various inhalation or
intravenous drugs. If the patient is awake, the patient can respond and report symptoms of preterm
labor, fetal heart rate should have little variability, and the patient will be mobilized more quickly. Early
mobilization will decrease the risk of a thromboembolic event.
78. What is the leading cause of maternal death?
The leading cause of maternal death is major trauma. Fetal loss in this situation is directly related to
the timing of maternal death and fetal maturity at the time of the traumatic event.
79. What are the reasons for emergent caesarean section?
The reasons for emergent C-section are:
• Astablemotherwithfetaldistress
• Uterinerupture
• Graviduterussizepreventingnecessaryabdominalsurgery
• Agravidmother’slifeisindangerandcannotbesaved(e.g.,trauma)
80. Is it possible to prevent HIV transmission to the fetus from an HIV positive gravid
mother?
Yes. Combination medical therapy throughout pregnancy is recommended to prevent transmission to
the fetus.
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81. What is the percentage of pregnant patients who undergo nonobstetric surgery?
The statistics show approximately 0.2% to 1% of pregnant patients will undergo a surgical procedure
unrelated to pregnancy.
82. What are the most common nonobstetric surgeries performed on a pregnant
woman?
The most common nonobstetric procedure performed on a pregnant woman is an appendectomy,
followed by cholecystectomy.
83. What is considered the maximum fetal radiation exposure?
The maximum amount of radiation exposure considered safe for a fetus is 5.0 rad.
84. What is the amount of background fetal radiation exposure during a 9-month
pregnancy?
The average amount of background fetal radiation during 9 months of pregnancy is approximately 0.3
to 0.9 rad.
85. What are the possible or potential concerns with excess fetal radiation?
The theoretical concerns with excess fetal radiation are abortion, birth defects, and future risk of can-
cer throughout life. These concerns make it important to use radiation as a diagnostic modality only if
completely necessary.
86. What amount of radiation is associated with fetal loss?
The cause of fetal loss seems to be an absolute threshold phenomenon. If a fetus receives 10 rad of
radiation or greater during the first 8 weeks of gestation, it will result in the loss of the fetus.
Most diagnostic imaging exposes fetus with 0.0007 (Chest X-ray) to 0.4 rad (Arteriogram) of
radiation. (A head CT exposes the fetus to 0.0013 rads.)
87. Do ultrasounds or MRI have any deleterious effects on the fetus?
MRI and ultrasound are considered safe imaging modalities during pregnancy. When performing an
MRI, gadolinium should be avoided due to its uptake in the amniotic fluid. This uptake may have an
effect on the fetus; however the possible effect is unknown.
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Management Considerations to Patients with Endocrine Diseases
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Clark OH: Thyroid & parathyroid (Chapter 16). In Doherty GM, editor: Current diagnosis & treatment: surgery, ed 13, New
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Management Considerations to the Pregnant Patient
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MANAGEMENT OF THE
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DIABETIC PATIENT
Samir Singh, Bradley A. Gregory
CHAPTER 21
1. What is diabetes?
Diabetes is a chronic metabolic disorder resulting in hyperglycemia from defects in insulin secre-
tion, insulin action, or both. Diabetes creates a physiologic predisposition for developing generalized
microvascular, macrovascular, and neuropathic complications.
2. How is glucose normally metabolized?
Glucose absorbed after a meal enters the circulation of the hepatic portal system and is taken to the
liver where about 30% of all ingested glucose is metabolized. The remaining glucose continues in the
bloodstream for distribution to other organs and tissues. Blood glucose levels are normally maintained
between 60 and 130 mg/dL. Excess glucose is converted to glycogen (glycogenesis) stored mostly
in liver and muscle and triglycerides stored in adipose tissue (lipogenesis). If plasma glucose
concentrations decrease, the body breaks down glycogen to glucose (glycogenolysis).
During energy deprivation states, triglycerides (omega-3 fatty acids attached to glycerol) are
broken down into glycerol and fatty acids (lipolysis), which are converted to glucose. Amino acids can
be converted to glucose in the liver through gluconeogenesis.
3. How does insulin facilitate uptake of glucose into cells?
Insulin is released in a rapid surge during the first 10 to 30 minutes after a meal. This is followed
by a second phase of a slower, sustained release of insulin. Insulin receptors in the cell membrane
have alpha and beta subunits. Insulin binds to subunit alpha, which causes a change in subunit beta.
Subunit beta promotes the activity of the enzyme tyrosine kinase that phosphorylates intracellular
insulin receptors (insulin-receptor substrates). This activates second messenger pathways that alter
existing protein and protein synthesis. The net result is a change in cell metabolism that brings
glucose into the cell via GLUT transporters.
4. From where is insulin secreted?
Insulin is secreted from the beta cells of the endocrine pancreas during the fed state when blood
glucose concentrations rise above 100 mg/dL or with increased parasympathetic activity.
5. How does insulin lower the plasma glucose?
• Insulinpromotesglucoseuptakeintomosttissues.Targettissuesforinsulinaretheliver,adipose
tissue, and skeletal muscles. Other tissues, including the brain and transporting epithelia of the
kidney and intestine, do not require insulin for glucose uptake and metabolism.
• Insulinenhancescellularutilization(glycolysis),storageofglucose(glycogenesis),andfatsynthesis
(lipogenesis). Insulin simultaneously inhibits glycogen breakdown (glycogenolysis), glucose synthesis in the liver (gluconeogenesis), and fat breakdown (lipolysis).
• Insulinenhancesutilizationofaminoacidsinproteinsynthesisandinhibitsproteinbreakdown.
• Insulinpromotesfatsynthesisbyinhibitingbetaoxidationoffattyacidsandpromotingconversion
into triglycerides (lipogenesis).
6. From where is glucagon secreted?
Glucagon is secreted from alpha cells of the endocrine pancreas during the fasted state when blood
glucose concentrations fall below 100 mg/dL or with increased sympathetic activity. It is also found in
the alpha cells of the stomach.
7. What metabolic effects does glucagon regulate?
The metabolic effects exerted on the liver, muscle, and adipose tissue are antagonistic to those
of insulin. Glucagon mobilizes stored energy by promoting glycogenolysis (especially at the liver),
gluconeogenesis, and lipolysis by activating hormone-sensitive lipase. Other effects of glucagon
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include stimulating the secretion of insulin by increasing plasma glucose and stimulating the secretion
of growth hormone.
8. How is cortisol secreted and regulated?
Cortisol is a glucocorticoid released in response to stress and low blood glucose. The control pathway
for cortisol secretion is known as the hypothalamic-pituitary-adrenal (HPA) pathway. Corticotropinreleasing hormone (CRH) is released from the hypothalamus. CRH stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. ACTH stimulates cortisol release from the
zona fasciculata of the adrenal cortex, which in turn causes negative feedback to CRH and ACTH.
9. What metabolic role does cortisol play in glucose metabolism?
Overall cortisol is catabolic and prevents hypoglycemia. It promotes gluconeogenesis in the liver,
breakdown of skeletal muscle proteins into pyruvate and lactate, which facilitate gluconeogenesis,
and enhances lipolysis. The glycerol from fatty acids can be used for gluconeogenesis.
10. How does epinephrine exert its metabolic controls?
Effects are mediated through both alpha-1 and beta-2 receptors. Alpha-1 receptors of the pancreas
promote glucagon release from the alpha cells of the pancreas and inhibit insulin secretion at
the beta cells of the pancreas. Beta-2 receptor agonism results in lipolysis, gluconeogenesis, and
glycogenolysis.
11. What is the role of epinephrine in glucose regulation?
The overall goal of epinephrine is to protect plasma glucose levels. In the muscle and liver, it promotes
glycogenolysis and gluconeogenesis as well. Additionally, it will inhibit insulin release and stimulate
glucagon release through alpha-1 receptors in the pancreas. In the bloodstream, it will inhibit glucose
uptake. Finally, epinephrine stimulates hormone-sensitive lipase to facilitate lipolysis in muscle and
adipose tissue.
12. What is the role of growth hormone in glucose regulation?
Growth hormone is an anabolic hormone secreted by cells in the anterior pituitary gland. It is secreted
by stimuli such as exercise-induced hypoglycemia, fasting, and stress from trauma, fever, and surgery. Growth hormone counteracts, in general, the effects of insulin on glucose and lipid metabolism.
Growth hormone release is inhibited by glucose and free fatty acids. Growth hormone also increases
plasma glucose, mobilizes free fatty acids and protein stores, lipolysis, glycogenolysis, and inhibits
glucose uptake by muscle and adipose tissue.
13. What is the role of thyroid hormone in glucose regulation?
Triiodothyronine (T3), which is the metabolically active form of thyroid hormone, and thyroxine (T4),
which is the prohormone, both act to raise blood glucose. They do so by enhancing glycogenolysis and
by enhancing protein metabolism and absorption of glucose from the intestines.
14. What are the four different types of diabetes mellitus?
• Type 1 diabetes (insulin-dependent diabetes mellitus or IDDM). Characterized by a severe de-
ficiency of insulin due to autoimmune destruction of beta cells of the pancreas. This form accounts
for <10% of all cases of diabetes mellitus. It is usually associated with young people, but can occur
at any age. These patients require insulin to maintain glucose homeostasis.
• Type 2 diabetes (noninsulin-dependent diabetes mellitus or NIDDM). Initially characterized by
insulin resistance secondary to environmental and genetic factors, followed by failure of beta cells
of the pancreas to compensate for the increased insulin requirements. It accounts for >90% of all
cases of diabetes mellitus. It is usually a disease of adulthood; however, it is being increasingly diagnosed in younger age groups. Therefore their muscle and adipose cells cannot transport glucose.
• Gestational diabetes. Complicates up to 4% of all pregnancies. It typically resolves after delivery;
however, up to 40% of women with gestational diabetes will develop type 2 diabetes within
10 years of developing gestational diabetes.
• Secondary diabetes. Diabetes that results from genetic defects in insulin secretion or action,
exocrine pancreatic disease, pancreatectomy, endocrinopathies (e.g., Cushing’s syndrome, acromegaly), drugs, and other syndromes.
15. What are the hallmark symptoms of diabetes?
Polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (excessive eating/hunger).
Other symptoms may include fatigue, weight loss, blurred vision, fungal infections, and neuropathy of
hands and feet.
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16. What is the pathogenesis of type 1 diabetes?
Overt signs of type 1 diabetes do not typically appear until about 90% of beta cells are destroyed.
• Agenetic susceptibility predisposes some people to autoimmunity against beta cells of the
pancreas.
• Autoimmunity develops spontaneously or, more commonly, is stimulated by an environmental agent.
• Environmental injury can damage beta cells, which are then recognized as foreign by the immune
defenses.
17. What is the pathogenesis of type 2 diabetes?
• Obesityisthegreatestriskfactor.Itdoesnotcausediabetesbutcanunmaskit.Itisassociated
with increased plasma levels of free fatty acids, which make muscles more insulin resistant, causing decreased glucose uptake.
• Insulinproductiondecreaseswithage.
• Geneticsplaysasignicantbutpoorlyunderstoodrole.
• Lackofcompensationintype2diabeticsfromfailureoffreefattyacidstostimulatepancreatic
insulin secretion. Therefore, compensation does not occur, and hyperglycemia develops. Beta cells
become desensitized to glucose, leading to decreased insulin secretion.
18. What metabolic abnormalities are associated with type 1 diabetes?
Abnormalities are classified into those of carbohydrate, protein, and lipid metabolism.
• Type1patientsgenerallyhaveacombinationofglucoseunderutilizationandexcessiveglucosepro-
duction resembling the fasting state. Glucose is unable to get into certain tissues, which causes the
renal threshold to be surpassed, resulting in polyuria. Polyuria leads to dehydration, which triggers
polydipsia. In addition, because cells are not getting nourishment, patients experience polyphagia.
• Thesepatientsbreakdownproteinfrommuscletomakeglucose.Proteinsarerequiredforanti-
body production, white blood cell production, and healing of wounds. Deficiency of these proteins
leads to susceptibility of infections and poor wound healing.
• Insulindeciencyleadstolipolysisoftriglyceridesintofreefattyacids.Excessivefattyacid
breakdown leads to beta oxidation in the liver, creating acidic ketone bodies (acetoacetic acid and
beta-hydroxybutyric acid). Ketone bodies enter the blood and cause a type of metabolic acidosis.
19. What metabolic abnormalities are associated with type 2 diabetes?
The metabolic abnormalities are classified as insulin resistance, loss of sensitivity of cells to insulin,
and a decrease in insulin secretion. Insulin is unable to get into cells because either a post-receptor
defect prevents uptake or there is a problem of insulin binding to target cells in the liver, muscle, and
adipose tissue. In addition, type 2 diabetics may have a gradual decrease in basal levels of insulin
secretion because the pancreas loses sensitivity to glucose level changes.
20. What is diabetic ketoacidosis?
Diabetic ketoacidosis (DKA) is an acute, life-threatening medical emergency that can occur in
type 1 and type 2 diabetic patients (more commonly in type 1). DKA is the result of severe insulin
deficiency coupled with an absolute or relative increase of glucagon, which contribute to accelerated ketogenesis and severe hyperglycemia. Diagnostic criteria of DKA include blood glucose levels
>450 mg/dL, metabolic acidosis (pH <7.3), serum bicarbonate <15 mEq/L, ketonemia, and ketonuria.
Clinical manifestations include nausea and vomiting, Kussmaul respirations (rapid, deep breathing)
to reduce carbon dioxide levels in blood, abdominal pain, fruity acetone breath odor, altered mental
status/coma, dehydration, and tachycardia. Goals of treatment are fluid replacement initially using
0.9% normal saline intravenously (add 5% glucose once blood glucose reaches 250 mg/dL to prevent
hypoglycemia) and administration of insulin after confirming patient is not hypokalemic (0.1 u/kg of
regular insulin followed by infusion of 0.1 units/kg/hr); monitor and replace potassium, magnesium,
and phosphate within 1 to 2 hours of starting insulin. Bicarbonate replacement is controversial and not
necessary in most cases.
Complications of treatment of DKA include cerebral edema if glucose levels decease too rapidly,
hyperchloremic non-gap metabolic acidosis due to rapid infusion of normal saline, cardiac arrhythmias, and death.
21. What is hyperosmolar hyperglycemic nonketotic coma?
Hyperosmolar hyperglycemic nonketotic coma (HHNS) is a state of severe hyperglycemia
(>600mg/dL), hyperosmolarity (>320 mOsm/L) and dehydration. It usually occurs in patients who are
type 2 diabetics, age 65 or older. It is less common than DKA, but it carries a higher mortality rate.
CHAPTER 21 MANAGEMENT OF THE DIABETIC PATIENT 221
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Low insulin levels lead to hyperglycemia, causing osmotic diuresis and dehydration. Ketogenesis
is minimal because a small amount of insulin is released to blunt counterregulatory hormone release
(glucagon). Ketosis and acidosis are typically minimal or absent. The symptoms may go unrecognized for weeks. Key features of HHNS are severe hyperosmolarity (>320 mOsm/L), hyperglycemia
(>600 mg/dL), dehydration, and the absence of acidosis and ketosis (unlike DKA). BUN is usually
elevated with other laboratory findings consistent with prerenal azotemia. The treatment involves
fluid replacement with normal saline (1 L in the first hour followed by another liter in the next
2 hours. Switch to 5% glucose in one-half normal saline once blood glucose reaches 250 mg/dL) and
administration of insulin (initial bolus of 5 to 10 units intravenously, followed by a low-dose infusion of
2 to 4 units/hour). Complications include cerebral edema from rapid lowering of glucose, exacerbation
of CHF in predisposed patients, cardiac arrhythmias, and death.
22. What tissues do not require insulin for glucose transport?
• Nervoustissue
• Brain
• Lensoftheeye
• Bloodvessels
• Kidneytubules
23. What are the major chronic complications of diabetes?
• Neuropathy(peripheralneuropathy[feetandhands],cranialnervecomplications[mostoften
involvesCNIII,IV,VI],mononeuropathies[mediannerve,ulnarnerve,commonperoneal],and
autonomicneuropathy[impotence,neurogenicbladder,gastroparesis,constipation,postural
hypotension])
• Retinopathy(nonproliferativeretinopathymostcommon[funduscopicexamshowshemorrhages,
exudates,microaneurysms,andvenousdilation]andproliferativeretinopathy[showsneovascularizationandscarring,canleadtoretinaldetachment,vitrealhemorrhage,andblindness])
• Macroangiopathy(acceleratedatherosclerosis,stroke,myocardialinfarction,peripheralvascular
disease)
• Nephropathy(nodularglomerularsclerosis[Kimmelstiel-Wilson syndrome],diffuseglomerular
sclerosis, isolated glomerular basement membrane thickening, microalbuminuria/proteinuria)
• Increasedsusceptibilitytoinfection(impairedWBCfunction,reducedbloodsupply,andneuropathy;
increased risk of cellulitis, candidiasis, pneumonia, osteomyelitis, and polymicrobial foot ulcers)
24. What are some of the ocular problems manifested in diabetic patients?
Cataracts, retinopathy, and glaucoma. Diabetic retinopathy is the leading cause of blindness in the
United States.
25. What biochemical pathways are suspected of contributing to diabetic
complications?
The suspected pathways are enzymatic glycosylation and the buildup of sorbitol. Enzymatic
glycosylation is the process by which glucose attaches to proteins throughout the body at a rate
proportional to the plasma glucose concentration. The proteins glycosylated include serum albumin,
collagen, basic myelin protein, and low-density lipoproteins (LDLs). The function of the proteins is
altered.
Hyperglycemia leads to buildup of glucose in tissues that do not require insulin for uptake.
Excess glucose is metabolized to sorbitol, which creates an osmotic gradient favoring water diffusing
into the cell.
26. What is the enzyme that is responsible for the breakdown of glucose into
sorbitol?
Aldose reductase.
27. How do advanced glycosylation end-products (AGEs) contribute to diabetic
complications?
AGEs are the result of enzymatic glycosylation. They get incorporated into the collagen that comprises
the basement membranes of capillaries located in the eye, kidney, nerves, and skin. This results in
thickening of basement membranes and a reduction in production of relaxing factors by the endothelium, causing vasoconstriction and, ultimately, hypertension. In addition, AGEs irreversibly attach to
collagen walls in larger vessels. This impedes the normal efflux of LDLs entering the vessel wall and
promotes cholesterol deposition.
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