<< . .

( 87)

. . >>

Chapter 14

Table 14.10 Adjustment of drug dosages in renal failure Beta-blockers Down-titrate dose.
Alpha-blockers No change in dose required.
Fentanyl No change in dose required.
Calcium channel No change in dose required.
Alfentanil No change in dose required.
Remifentanil No change in dose required.
Methyldopa Excreted unchanged in urine.
Morphine Metabolites morphine 3- and 6-glucuronide
Prolonged duration of action.
accumulate and cause prolonged effect.
Antidysrhythmics No change in dose required.
Not cleared by hemofiltration or dialysis.
Digoxin Reduce dose and monitor serum
Diamorphine Metabolites accumulate and cause prolonged
Ranitidine Reduce dose by half when GFR < 10 ml/min.
Meperidine Metabolite (normeperidine) accumulates and
Metoclopramide No need to reduce dose after single
may cause seizures.
administration only.
Codeine Accumulation of morphine metabolites may
Penicillins Reduce dose by half when GFR < 10 ml/min.
cause prolonged effects.
Cephalosporins Reduce dose by half when GFR < 10 ml/min.
Dihydrocodeine Accumulation of morphine metabolites may
Oxytocin Rapidly inactivated by the liver.
cause prolonged effects.
Caution with infusions, which can cause water
Dextropropoxyphene Accumulation can cause unwanted effects.
Buprenorphine Metabolites do not cause undesirable effects.
Ergometrine Metabolized in the liver and mainly excreted
Oxycodone Decrease dose by half in severe renal
in the feces.
No change in dose required.
Propofol No change in dose required. Glucuronide
Low molecular weight Reduce dose when GFR < 30 ml/min.
metabolites accumulate, but have no
unwanted effects.
Thiopental No change in dose required. GFR ¼ glomerular filtration rate; NSAID ¼ nonsteroidal anti-
Ketamine No change in dose required. inflammatory drug
Volatile anesthetic Some renal metabolism but mainly pulmonary
agents excretion, so generally safe to use.
All decrease GFR but have no effect on renal
severe on the side of the rupture. Five patients required nephrect-
omy, one died before surgery, and two suffered intrauterine fetal
Renal blood flow maintained with halothane,
isoflurane, and desflurane.
Sevoflurane should be avoided because of
potential renal toxicity of fluoride ion. Reflux nephropathy and calculi
Succinylcholine No change in dose required. Reflux nephropathy and renal scarring are important causes of
Atracurium No change in dose required. renal impairment in pregnancy. Scarring occurs in 50% of women
Vecuronium, Best avoided, because all have partial renal who have bacteruria in pregnancy, and UTI is more common if
Rocuronium excretion. vesico-ureteric reflux is present. Renal stones are no more com-
Pancuronium If used, may have prolonged action and mon in pregnancy, because inhibitors such as magnesium,
neuromuscular block must be monitored. citrate, and nephrocalcin are present in greater quantity. Apart
Neostigmine Excretion delayed, similar to nondepolarizing from an increase in UTI, stones do not have an adverse impact on
muscle relaxants. pregnancy. Nevertheless, treatment may be difficult, because
Diazepam Metabolites accumulate and may cause xanthine oxidase inhibitors for urate stones, and d-penicillamine
prolonged effects. for cystine stones, are best avoided, especially in the first trime-
Midazolam Reduce dose if GFR < 10 ml/min. ster. There are inadequate data on the safety of lithotripsy during
Paracetamol Accumulates, but normal dose suitable. pregnancy. It has been suggested that some women with severe
NSAID Avoid, as they cause a rapid decrease in GFR in vesico-ureteric reflux might benefit from ureteric reimplantation
patients with renal disease. Also cause prior to pregnancy and that early dialysis may improve fetal
hyperkalemia, edema and hypertension. outcome.
Not removed by hemofiltration or dialysis. Ureteric obstruction and subsequent hydronephrosis, in the
Tramadol Active metabolites may accumulate. absence of renal calculi, can occur from pressure by the expand-
Reduce dose or increase dosing frequency in ing uterus. This can cause severe maternal flank pain and may
severe renal impairment. require ureteric stent placement to relieve the obstruction.
Butyrophenones No change in dose required. Cystoscopy and stent placement can be performed under spinal
Phenothiazines No change in dose required. anesthesia. Figure 14.1 shows an x-ray of an indwelling left ure-
Clonidine No change in dose required. teric stent in a woman with ureteric compression and hydrone-
Glyceryl trinitrate No change in dose required. phrosis at 36 weeks™ gestation.

4 Metabolic disorders

Patients with Churg-Strauss syndrome develop worsening
asthma, eosinophilia, and granulomatous lesions, but as the
disease mostly affects males, pregnancy is rare.108 Women with
Wegener granulomatosis show signs of upper respiratory tract
disease, including epistaxis and nasal bridge collapse,109 and
ARF may develop.
Treatment of these conditions involves high-dose cyclophos-
phamide and corticosteroids. Plasma exchange may improve
outcome but mortality is high. For patients who enter remission
within four to six weeks, the ANCA status may become negative.
Pregnancy is best avoided until the disease is in remission, since
pregnancy may cause a relapse. The placenta appears unaffected
by the vasculitic process, so fetal mortality and morbidity is low.

Hemolytic uremic syndrome (see Chapter 17)
Hemolytic uremic syndrome (HUS) is characterized by nonim-
mune hemolytic anemia, thrombocytopenia, and renal failure.
The incidence of HUS during pregnancy is estimated as 1 in
25 000. Hemolytic uremic syndrome in pregnancy is associated
with a high perinatal mortality rate.110 For further details please
refer to Chapter 17.

Goodpasture syndrome
Goodpasture syndrome is an autoimmune disease in which anti-
glomerular basement membrane antibodies are directed against
collagen IV in basement membranes. It is characterized by glo-
merulonephritis and pulmonary hemorrhage. It is mainly a dis-
Figure 14.1 Plain x-ray of abdomen and pelvis in a woman at 36 weeks™
ease of young men, or men and women over 60 years of age.
gestation with severe flank pain associated with left ureteric obstruction and
Younger patients present with hemoptysis, anemia, proteinuria,
hydronephrosis. A left ureteric stent was placed under spinal anesthetic. The stent
and red-cell casts in the urine. Management includes glucocorti-
and a fetus with a head engaged in the pelvis are clearly seen. The arrow points at
coids (to control pulmonary hemorrhage), immunosuppression
the left ureteric catheter. (See color plate section.)
(to prevent further renal damage), and intermittent plasma-
Glomerulonephritis pheresis (to clear circulating antibasement membrane anti-
bodies from the circulation). The disease usually displays a
The label ˜˜glomerulonephritis™™ encompasses a range of conditions
chronic course, with recurrence or complete clearance of the
in which the glomerulus is inflamed (see Table 14.11), either as a
antiglomerular basement membrane antibody following treat-
primary renal disease or part of a systemic illness. Diagnosis and
ment. Autoimmune antibodies can be deposited in the placenta.
division into pathological subcategories requires renal biopsy,
which has a low complication rate in pregnancy.105 Patients pre- Goodpasture syndrome is rare in pregnancy but cases
have been reported.111,112 Pregnancy may be complicated by
sent with nephrotic syndrome (proteinuria, edema, and hypoalbu-
glucocorticoid-induced hyperglycemia, hemodialysis, intermit-
minemia); nephritic syndrome (oliguria, edema, hypertension,
tent plasmapheresis, immunosuppressant therapy, and preterm
proteinuria, hematuria, and renal impairment); or proteinuria,
birth.111 Successful pregnancy was reported in a woman follow-
hematuria, or hypertension alone. Pregnancy outcome is deter-
ing kidney transplantation for end-stage renal failure. This
mined by the severity of renal impairment. Patients with lupus
patient had no pulmonary involvement but experienced pre-
nephritis have a high rate of fetal loss and deterioration in renal
function, particularly if the disease is active.106 Postinfectious glo- eclampsia and graft rejection postpartum, probably from poor
compliance with immunosuppressive therapy.112
merulonephritis is unusual in pregnancy, but can occur after strep-
tococcal throat infection.107 It presents with an acute nephritic
syndrome, characterized by severe hypertension and edema. The
Inherited renal disorders
prognosis is good and treatment is mainly supportive, including
Autosomal dominant polycystic kidney disease (ADPKD)
antihypertensive drugs and diuretics.
In autosomal dominant polycystic kidney disease (ADPKD) renal
Vasculitic diseases cyst enlargement leads to destruction of surrounding renal tis-
Wegener granulomatosis and Churg-Strauss syndrome are small sue, resulting in renal failure, and bilateral kidney enlarge-
ment.113 Presenting symptoms include hypertension, UTI,
vessel vasculitides associated with antineutrophil cytoplasmic
antibodies (ANCA). Blood-vessel walls become inflamed and hematuria, loin pain, and renal calculi, but the first manifesta-
necrotic, leading to fever, night sweats, and weight loss. tion is often end-stage renal failure. Cysts may be found in the

Chapter 14

Table 14.11 Glomerulonephritis

Condition Clinical presentation Renal prognosis Treatment

Minimal change Often presents in childhood with nephritic Rarely progresses to renal >90% respond to high-dose
nephropathy syndrome. dysfunction. corticosteroids.
Occasionally secondary to NSAID use or
Focal segmental Nephritic syndrome. 50% patients develop end-stage High-dose corticosteroids.
glomerulosclerosis Hypertension, microscopic hematuria, renal failure within ten years. ACE inhibitor to reduce
impaired renal function are associated. proteinuria.
Statin for hyperlipidemia.
Membranous Asymptomatic proteinuria or nephritic Impaired renal function may May resolve completely if
nephropathy syndrome. Microscopic hematuria and occur. causative agents withdrawn.
hypertension are associated. 25% patients have resolution of
May have IgG complex deposition. proteinuria.
Idiopathic or secondary to NSAID, gold, High risk of thrombotic effects.
penicillamine, carcinoma of breast,
bronchus, colon.
IgA nephropathy Most common cause of hematuria worldwide. Good prognosis in patients with Immunosuppression not helpful.
Deposition of IgA in glomerulus. Similar no proteinuria, hypertension, No proven treatment.
glomerular injury is seen in Henoch or renal impairment.
Schonlein purpura, with vasculitic rash 25% of patients with proteinuria
and arthritis. of 1 g per 24 h develop end-
stage renal failure.
Mesangiocapillary Uncommon. Up to 50% develop renal failure
glomerulonephritis Three sub-types. within ten years.
Associated with activation of the
complement cascade.
Proteinuria, hematuria, hypertension,
impaired renal function.
Focal necrotizing Acute nephritic syndrome (acute renal failure, Usually presents with acute Plasma exchange to remove
glomerulonephritis hematuria, proteinuria, cellular casts in renal failure. circulating antibodies.
urine). Corticosteroids and
With pulmonary hemorrhage is known as cyclophosphamide.
Goodpasture syndrome. Æ ANCA.
May represent form of small vessel vasculitis.

NSAID ¼ nonsteroidal anti-inflammatory drugs; ACE ¼ angiotensin converting enzyme; ANCA ¼ antineutrophil cytoplasm antibodies

Tuberous sclerosis
liver and pancreas and other extrarenal complications include
intracranial aneurysms, mitral valve prolapse, and diverticular Tuberous sclerosis is an autosomal dominant multisystem dis-
disease. Clinical symptoms and evidence of renal dysfunction order in which hamartoma formation affects the skin, brain, and
heart in particular.115,116 Features include seizures, mental retar-
usually appear in later life, but pregnancy outcomes of 235
women with ADPKD have been described.114 A decline in renal dation, facial angiofibromas, and renal angiomyolipomas. Only
function was associated with increasing multiparity and although 23 pregnancies in women with tuberous sclerosis were identified
fertility was unaffected, ectopic pregnancy rates were higher. in 2005, and two were complicated by bleeding into renal
Twenty five percent of affected women developed hypertension
during pregnancy, 11% preeclampsia, and there was an increased
Alport syndrome
risk of subsequent chronic hypertension. Normotensive women
with normal renal function generally had uncomplicated preg- Alport syndrome is an inherited disease characterized by hema-
nancies. Increases in intracranial pressure should be avoided or turia, proteinuria, progressive renal failure, and sensorineural
deafness.116 Some patients also develop lenticonus of the anterior
attenuated because intracranial aneurysms may be present,
although rupture has not been reported. Epidural analgesia with lens capsule, retinopathy, and rarely mental retardation and leio-
controlled instrumental delivery, or elective C/S, is a good man- myomatosis. A variety of related syndromes reflect the many
agement option. genetic variations “ examples are X-linked, recessive, dominant,

4 Metabolic disorders

regular menses.124 Diagnosis of pregnancy can be difficult, as small
benign familial hematuria, and nail-patella syndrome. Renal fail-
ure often develops by 30 years of age. amounts of human chorionic gonadotrophin (HCG) are secreted
by somatic cells and are not cleared by the kidney, producing
Bartter syndrome elevated levels in the nonpregnant state. Longstanding proteinuria
Bartter syndrome is a rare, autosomal recessive renal tubular dis- can give false positive pregnancy tests.
order characterized by severe hypokalemia, metabolic alkalosis, Dialysis may be required in women with renal impairment who
hyperaldosteronism, and normotension.117 Clinical manifestations become pregnant and then develop end-stage renal failure. Some
include growth restriction, muscle weakness, cramps, polyuria, and recommend commencing dialysis when the GFR falls below
polydipsia. The limited number of case reports during preg- 20 ml/min. Protein restriction can be relaxed and may improve
nancy117,118,119,120,121 suggest good maternal and fetal outcome, maternal and fetal nutrition. Better outcomes are generally seen
provided serum potassium and magnesium levels are normal. in women who reach later gestations before requiring dialysis,
Obstetric and anesthetic management should be directed and in those who have been on dialysis for shorter periods before
toward maintenance of serum potassium levels, using intravenous becoming pregnant.
potassium supplements and magnesium supplements, as Preterm delivery occurs in about 50% of cases, and for uncer-
required.119 In the nonpregnant population, angiotensin convert- tain reasons polyhydramnios is a common feature.124 Attention
ing enzyme (ACE) inhibitors are effective at maintaining normo- has been directed to improving outcome by increasing the time
kalemia, but are contraindicated during pregnancy because of the spent on dialysis, with the best results found in those who are
potential for both teratogenic (hypocalvaria) and fetal effects (renal dialyzed for 20 or more hours per week. Maternal hypertension
failure, oliguria, and demise). Potassium sparing diuretics such as occurs in 40“80% of dialyzed women and abruption, anemia,
amiloride and spironolactone are safe and good alternatives.120 and antepartum hemorrhage may occur. About 10% of women
Sodium loss is a feature of Bartter syndrome, so patients are develop preeclampsia, and hypertension worsens in 20%.
prone to hypovolemia. Regional block should be established care- Increased red blood cell production during pregnancy is out-
fully, with preparation to prevent and treat hypotension. Marked stripped by the increase in plasma volume, so hemoglobin con-
resistance to vasopressors, especially angiotensin II and norepi- centration usually falls. Up to a two-fold increase in
nephrine, has been reported,119 and baroreceptor responses are erythropoietin dose may be required to maintain an adequate
often abnormal. If blood loss is anticipated, CVP monitoring is level of hemoglobin.
advisable. Hyperventilation should be avoided because hypo- Successful pregnancy among patients on continuous ambula-
tory peritoneal dialysis (CAPD) has also been reported.124
capnia may lead to a reduction in serum potassium. Effective
regional analgesia for laboring patients is recommended. Continuous ambulatory peritoneal dialysis may be complicated
by premature labor precipitated by peritonitis. A theoretical
Gitelman syndrome advantage over hemodialysis is that the fetus is exposed to a
Gitelman syndrome is a milder form of Bartter disease that rarely more stable environment, with fewer rapid fluid and electrolyte
progresses to end-stage renal disease. Prolonged QT interval has shifts, but obstetric outcomes are similar. The C/S rate is approxi-
been described,122 so drugs prolonging the QT interval should be mately 50%, with many cases urgent because of premature rup-
used with caution and with appropriate monitoring (see ture of membranes or abruption. The anesthesiologist should
Chapter 2). liaise with the nephrologist to determine current fluid and elec-
trolyte status and time of last dialysis.
Renal tubular acidosis
Renal tubular acidosis is characterized by inadequate renal
hydrogen-ion excretion, despite normal glomerular filtration.
Type 1 renal tubular acidosis is inherited in an autosomal domi- Although the most common cause of hepatic dysfunction and
nant manner and affects the distal tubules, while Type 2 affects jaundice in pregnant women is viral hepatitis (A, B, C, D, E, and
the proximal tubules. Both result in hyperchloremic metabolic G viruses), there are a number of uncommon diseases unique to
acidosis, with a normal anion gap. pregnancy that are significant causes of mortality and morbidity.
There are few reports of renal tubular acidosis and pregnancy. The most important are intrahepatic cholestasis of pregnancy
One describes two pregnancies, both complicated by hyperten- and AFLP. Liver dysfunction is also a feature of many multisystem
sion123 although there were no adverse maternal or fetal sequelae. disorders, the most important of which is preeclampsia. The
obstetric anesthesiologist has a role to play in antenatal, intrapar-
tum, and postpartum multidisciplinary care and should have a
Renal replacement therapy (dialysis) in the
sound understanding of the pathophysiology of these conditions.
pregnant woman with renal disease
Regional analgesia and anesthesia is often valuable, but dys-
Although still uncommon, the incidence of pregnancy in women function of the coagulation system may preclude neuraxial tech-
who receive chronic hemodialysis is 1“7%, and 30“50% of these niques. General anesthesia should be modified to address
women will have a successful pregnancy outcome. Improvements considerations relevant to patients with impaired liver function.
in dialysis regimens and the widespread use of erythropoietin have Women with cirrhosis, portal hypertension, acute liver failure, or
led to less anovulation and infertility such that many women have hepatic rupture pose major anesthetic challenges.

Chapter 14

Although ARF in pregnancy is a rare event, acute tubular necro- 18. Dann, A. T., Kenyon, A. P., Seed, P. T. et al. Glutathione S-transferase and
liver function in intrahepatic cholestasis of pregnancy and pruritus gravi-
sis and/or renal cortical necrosis are associated with several
darum. Hepatology 2004; 40: 1406“14.
common diseases of pregnancy, including severe preeclampsia
19. Fisk, N. M. & Storey, G. N. Fetal outcome in obstetric cholestasis. Br. J.
and PPH. Acute renal failure is also associated with a number of Obstet. Gynaecol. 1988; 95: 1137“43.
less common diseases, such as AFLP and obstructive uropathy. 20. Kondrackiene, J., Beuers, U. & Kupcinskas, L. Efficacy and safety of urso-
Maternal and fetal outcomes in women with renal disease depend deoxycholic acid versus cholestyramine in intrahepatic cholestasis of preg-
nancy. Gastroenterology 2005; 129: 894“901.
on factors such as degree of renal dysfunction at conception, the
21. Riely, C. A. & Bacq, Y. Intrahepatic cholestasis of pregnancy. Clin. Liver Dis.
underlying disease process, and the degree of hypertension.
2004; 8: 167“76.
Improvements in medical care now result in successful preg- 22. Davies, M. H., da Silva, R. C., Jones, S. R. et al. Fetal mortality associated with
nancy outcomes, even among women receiving renal replace- cholestasis of pregnancy and the potential benefit of therapy with urso-
ment therapy. These women should be identified as high risk deoxycholic acid. Gut 1995; 37: 580“4.
23. Kowdley, K. V. Lipids and lipid-activated vitamins in chronic cholestatic
early in pregnancy, and managed in a tertiary center with appro-
diseases. Clin. Liver Dis. 1998; 2: 373“89.
priate monitoring and care plans established in liaison with peri-
24. Yarnell, R. W. & D™Alton, M. E. Epidural hematoma complicating cholestasis
natologists and nephrologists. The general principles relevant to of pregnancy. Curr. Opin. Obstet. Gynecol. 1996; 8: 239“42.
anesthesia for patients with renal impairment or failure can be 25. Schumann, R. & Hudcova, J. Cholestasis of pregnancy, pruritus and
applied during pregnancy. 5-hydroxytryptamine 3 receptor antagonists. Acta Obstet. Gynecol. Scand.
2004; 83: 861“2.
26. Castro, M. A., Fassett, M. J., Reynolds, T. B. et al. Reversible peripartum liver
failure: a new perspective on the diagnosis, treatment and causes of acute
1. Baker, A. L. Liver and biliary tract diseases. In Barron, W. M. & Lindheimer, M. D. fatty liver of pregnancy, based on 28 consecutive cases. Am. J. Obstet.
Gynecol. 1999; 181: 389“95.
(eds)., Medical Disorders During Pregnancy. St. Louis: Mosby, 2000, pp. 330“54.
2. Benjaminov, F. A. & Heathcote, J. Liver disease in pregnancy. Am. 27. Doshi, S. & Zucker, S. D. Liver emergencies during pregnancy.
J. Gastroenterol. 2004; 99: 2479“88. Gastroenterol. Clin. N. Am. 2003; 32: 1213“27.
3. Sookoian, S. Liver disease during pregnancy: acute viral hepatitis. Ann. 28. Monga, M. & Katz, A. R. Acute fatty liver in the second trimester. Obstet.
Gynecol. 1999; 93: 811“13.
Hepatol. 2006; 5: 231“6.
4. Latham, P. S. Liver diseases. In Gleicher, N. et al. (eds.), Principles and 29. Reyes, H. Acute fatty liver of pregnancy: a cryptic disease threatening
Practice of Medical Therapy in Pregnancy. New York: McGraw-Hill mother and child. Clin. Liver Dis. 1999; 3: 69“81.
30. Flint Porter, T. Acute fatty liver of pregnancy. Ch. 36. In Dildy, G. A., 3rd (ed.),
Professional, 1998, pp. 1111“225.
Critical Care Obstetrics. Massachusetts: Blackwell Science, 2004, pp. 380“5.
5. Stamm, C. A. & McGregor, J. A. Hepatitis in pregnancy. Ch. 37. In Dildy,
G. A., 3rd (ed.), Critical Care Obstetrics. Massachusetts: Blackwell Science, 31. Ko, H. & Yoshida, E. M. Acute fatty liver of pregnancy. Can. J. Gastroenterol.
2004, pp. 333“7. 2006; 20: 25“30.
32. Usta, I. M., Barton, J. R., Amon, E. A., Gonzalez, A. & Sibai, B. M. Acute fatty
6. Scully, L. J. Hepatitis. Ch. 10. Gastrointestinal and liver disease. In Lee, R. V.,
Rosene-Montella, R., Barbour, L. A., Garner, P. R. & Keely, E. (eds.), Medical liver of pregnancy: an experience in the diagnosis and management of
Care of the Pregnant Patient. Philadelphia, PA: American College of fourteen cases. Am. J. Obstet. Gynecol. 1994; 171: 1342“7.
Physicians-American Society of Internal Medicine, 2000, pp. 563“84. 33. Schoeman, M. N., Batey, R. G. & Wilcken, B. Recurrent acute fatty liver of
pregnancy associated with a fatty acid oxidation defect in the offspring.
7. Airoldi, J. & Berghella, V. Hepatitis C and pregnancy. Obstet. Gynecol. Surv.
2006; 61: 666“72. Gastroenterology 1991; 100: 544“8.
8. Kumar, G. P., Bhat, V. J. & Sowdi, V. Fulminant hepatic failure following 34. Jamerson, P. A. The association between acute fatty liver of pregnancy and
halothane anaesthesia. J. Clin. Forensic Med. 2005; 12: 271“3. fatty acid oxidation disorders. J. O. G. G. N. 2005; 34: 87“92.
35. Moldenhauer, J. S., O™Brien, J. M., Barton, J. R. & Sibai, B. Acute fatty liver of
9. Gonzalo Pascual, V., Forner Gonzalez, A., Salvador, E. et al. Severe acute
hepatitis after anesthesia with sevoflurane. Gastroenterol. Hepatol. 2005; 28: pregnancy associated with pancreatitis: a life threatening complication.
361“2. Am. J. Obstet. Gynecol. 2004; 190: 502“5.
36. Ockner, S. A., Brunt, E. M., Cohn, S. M. et al. Fulminant hepatic failure
10. Cheung, R. C., McAuley, R. J. & Pollard, J. B. High mortality rate in patients
with advanced liver disease independent of exposure to general anesthesia. caused by acute fatty liver of pregnancy treated by orthoptic liver trans-
J. Clin. Anesth. 2005; 17: 172“6. plantation. Hepatology 1990; 11: 59“64.
11. Nelson-Piercy, C. Hyperemesis gravidarum and total parenteral nutrition. 37. Amon, E., Allen, S. R., Petrie, R. H. & Belew, J. E. Acute fatty liver of preg-
nancy associated with preeclampsia: management of hepatic failure with
Ch. 10. Gastrointestinal and liver disease. In Lee, R. V., Rosene-Montella, R.,
Barbour, L. A., Garner, P. R. & Keely, E. (eds.), Medical Care of the Pregnant postpartum liver transplantation. Am. J. Perinatol. 1991; 8: 278“9.
Patient. Philadelphia, PA: American College of Physicians-American 38. Antognini, J. F. & Andrews, S. Anaesthesia for caesarean section in a patient
Society of Internal Medicine, 2000, pp. 545“63. with acute fatty liver of pregnancy. Can. J. Anaesth. 1991; 38: 904“7.
39. Corke, P. J. Anaesthesia for caesarean section in a patient with acute fatty
12. Outlaw, W. M. & Ibdah, J. A. Impaired fatty acid oxidation as a cause of liver
disease associated with hyperemesis gravidarum. Med. Hypotheses 2005; 65: liver of pregnancy. Anaesth. Intensive Care 1995; 23: 215“18.
1150“3. 40. Thomas, S. D. & Boyd, A. H. Prolonged neuromuscular block associated
with acute fatty liver of pregnancy and reduced plasma cholinesterase.
13. Selitsky, T., Chandra, P. & Schiavello, H. J. Wernicke™s encephalopathy with
Euro. J. Anaesthesiol. 1994; 11: 245“9.
hyperemesis and ketoacidosis. Obstet. Gynecol. 2006; 107: 486“90.
14. Chiossi, G., Neri, I., Cavazzuti, M. et al. Hyperemesis gravidarum compli- 41. Holzman, R. S., Riley, L. E., Aron, E. & Fetherston J. Perioperative care of a
cated by Wernicke encephalopathy: background, case report, and review of patient with acute fatty liver of pregnancy. Anesth. Analg. 2001; 92: 1268“70.
42. Servin, F., Cockshott, I. D., Farinotti, R. et al. Pharmacokinetics of propofol
the literature. Obstet. Gynecol. Surv. 2006; 61: 255“68.
15. Arrese, M. Cholestasis during pregnancy: rare hepatic diseases unmasked infusions in patients with cirrhosis. Br. J. Anaesth. 1990; 65: 177“83.
by pregnancy. Ann. Hepatol. 2006; 5: 216“18. 43. Gelman, S. General anaesthesia and hepatic circulation. Can. J. Physiol.
16. Pauli-Magnus, C. & Meier, P. J. Hepatocellular transporters and cholestasis. Pharmacol. 1987; 65: 1762“79.
44. Schmidt, C. C. Suttner, S. W., Piper, S. N. et al. Comparison of the effects of
J. Clin. Gastroenterol. 2005; 39: S103“S110.
17. Winton, G. B. & Lewis, C. W. Dermatoses of pregnancy. J. Am. Acad. desflurane and isoflurane anaesthesia on hepatocellular function assessed

<< . .

( 87)

. . >>

Copyright Design by: Sunlight webdesign