Critical Care Obstetrics part 39 pot

The goals of biliary surgery in cases of gallstone pancreatitis are to prevent recurrence and to decrease morbidity and mortality by removing the instigating agent.. While not indicated

cysts, hemorrhage, thrombophlebitis, and abcess formation [36] and provide guidance for directed sampling of abscess cavities (Figures 27.1 & 27.2 ) CT is also useful in differentiating pancre-atitis from other intra - abdominal pathologies

The role of ultrasound is typically quite limited in the initial evaluation of patients who have pancreatitis, because the pan-creas often is obscured by bowel gas Additionally, the panpan-creas may have an entirely normal sonographic appearance in the acute phase In patients suspected of having acute pancreatitis, the primary role of ultrasound is to assess for gallstones and biliary obstruction [36]

Differential d iagnosis

Abdominal complaints in pregnancy present unique diagnostic challenges (Table 27.3 ) Non - obstetric conditions include acute

rated these fi ndings, noting no difference in amylase activity

related to pregnancy Lipase levels were also studied, and no

signifi cant difference was found between the second and third

trimesters or compared with non - pregnant controls, although

one study noted a lower lipase level in the fi rst trimester [34]

Mean values of lipase in 175 women were approximately 12 IU/L,

with none exceeding 30 IU/L

As a screening tool for acute pancreatitis, urinary

trypsino-gen - 2 has also been evaluated in the trypsino-general population Using a

dipstick test for urinary trypsinogen - 2, Kemppainen et al [35]

evaluated 500 consecutive patients presenting to the emergency

room with abdominal pain The authors found 94% sensitivity

and 95% specifi city in detecting acute pancreatitis While

requir-ing further study, the 99% negative predictive value achieved with

this urinary dipstick test may prove a useful adjunctive test to

standard serum evaluation of amylase and lipase

Leukocytosis, hyperglycemia, hyperbilirubinemia, abnormal

coagulation tests, and elevated liver enzymes may also be present

Although other diseases can result in abnormal values, amylase

and lipase remain the cornerstone of diagnosis These values are

typically elevated more than threefold over normal

Radiologic e valuation

While the diagnosis of acute pancreatitis is based on clinical

sus-picion, physical examination, and elevated amylase and lipase,

radiologic tests aid in the confi rmation of acute pancreatitis and

can be used to monitor the development and progression of

complications A plain fi lm of the abdomen may show dilation

of an isolated loop of intestine (sentinel loop) adjacent to the

pancreas Pleural effusions may be detected on chest X - ray

Computed tomography (CT) is considered the radiographic

procedure of choice for determining the extent or the severity of

the pancreatitis [36] Since CT is unhindered by bowel gas

pat-terns, CT scans can demonstrate pancreatic necrosis,

pseudo-L

Figure 27.1 Computed tomography scan demonstrating necrosis in the head

of the pancreas (curved arrow) and free fl uid in the anterior pararenal space

(straight arrow) (Courtesy of Dr Paula Woodward.)

Figure 27.2 Computed tomography scan demonstrating pseudocyst in the tail

of the pancreas (arrow) (Courtesy of Dr Paula Woodward.)

Table 27.3 Differential diagnosis of acute pancreatitis

Non - obstetric conditions Acute cholecystitis Appendicitis Biliary colic Intestinal obstruction Duodenal ulcer Splenic rupture Mesenteric vascular occlusion Perinephric abscess Pneumonia Pulmonary embolus Myocardial infarction Diabetic ketoacidosis

Obstetric conditions Pre - eclampsia Ruptured ectopic pregnancy Hyperemesis gravidarum

atitis Utilizing color charts, Mayer and McMahon [43] identifi ed 90% of the patients who subsequently died and 72% of patients with severe morbidity

Biochemical indicators that have been evaluated as predictors

of severity of disease include C - reactive protein [44 – 46] , tryp-sinogen activation peptide [47 – 49] , procalcitonin [50,51] , throm-bomodulin [45] , and serum amyloid A [46] Only C - reactive protein is currently used clinically, but is limited in that it is predictive only after 48 – 72 hours following onset of symptoms While interleukin - 6, trypsinogen activation peptide and granulo-cyte nuclear elastase all show promise in acutely identifying patients destined for a severe clinical course, they await confi rma-tory trials and widespread acceptance into routine clinical use Compared with scoring systems and laboratory markers, con-trast - enhanced CT scans offer broader information regarding intra - abdominal anatomy Location and extent of necrosis are identifi ed and can be serially evaluated (see Figure 27.1 ) Infection within pseudocysts is suggested by evidence of gas production This test, however, may be limited in its availability and is diffi cult

to obtain in severely ill patients

cholecystitis, duodenal ulcer (including perforation),

appendici-tis, splenic rupture, perinephric abscess, mesenteric vascular

occlusion, pneumonia, diabetic ketoacidosis, biliary colic, and

intestinal obstruction In the pregnant patient, pre - eclampsia,

hyperemesis gravidarum, and ruptured ectopic pregnancy must

be added to the differential diagnosis

Preeclampsia may mimic pancreatitis with upper abdominal

pain, nausea, and vomiting Concomitant hypertension,

protein-uria, and edema, however, will usually be present Hyperemesis

gravidarum most often affects patients in the fi rst trimester,

without a signifi cant component of pain Ruptured ectopic

preg-nancy may produce symptoms similar to those seen in acute

pancreatitis Hemoperitoneum can occur with either and may

require laparotomy for diagnosis But ruptured ectopics are not

typically associated with an elevated lipase

Prognostic i ndicators

Several methods utilizing clinical and laboratory data have been

developed to indicate the severity of acute pancreatitis and allow

refi nement of prognosis [37 – 39] The most widely used criteria

were developed by Ranson (Table 27.4 ) The number of criteria

met correlates with the mortality risk for the individual For non

gallstone pancreatitis, patients with fewer than three signs have

rates of mortality less than 3% and morbidity less than 5%

Patients with three or more positive signs carry a 62% mortality

rate and a 90% morbidity rate Utilizing a modifi ed set of criteria

for gallstone pancreatitis, individuals with fewer than three signs

have a 1.5% mortality rate, while those with three or more signs

demonstrate a 29% mortality rate Critics of this system cite poor

sensitivity, specifi city, delayed assessment (due to the labs

required at 48 hours), and inability to perform repeated

assess-ments as major deterrents to its usefulness

Another method of clinically evaluating the severity of several

types of critical illnesses, including pancreatitis, is the Acute

Physiology and Chronic Health Evaluation (APACHE) III criteria

[40] Unlike Ranson ’ s criteria [37 – 39] , the APACHE assessment

[40] can be updated and the patient ’ s course monitored on a

continuing basis This system evaluates several variables, both

biochemical and physiologic, and calculates scores based on

devi-ation from normal values A 5 - point increase in score is

indepen-dently associated with a statistically signifi cant increase in the

relative risk of hospital death within a specifi c disease category

Within 24 hours of admission, 95% of patients admitted to the

intensive care unit could be given a risk estimate for death within

3% of that actually observed [40] Although more complex and

computer dependent, the APACHE scoring system appears more

accurate than Ranson ’ s criteria in predicting morbidity [41] The

addition of body mass index seems to improve prediction as

obesity predicts severity [42] Several single prognostic indicators

have been investigated in order to achieve early identifi cation of

pancreatic necrosis Paracentesis can be performed; return of

dark, prune - colored fl uid is characteristic of necrotizing

Table 27.4 Clinical indicators of poor prognosis: Ranson ’ s criteria [36 – 38] Non - gallstone pancreatitis

On admission

Within 48 h Decrease in hematocrit > 10% Increase in BUN > 5 mg/dL

P a O 2 < 60 mmHg Base defi cit > 4 mmol/L Fluid defi cit > 6 L

Gallstone pancreatitis

On admission

Within 48 h Decrease in hematocrit > 10% Increase in BUN > 2 mg/dL

Base defi cit > 5 mmol/L Fluid defi cit > 4 L AST, aspartate amino transferase; BUN, blood urea nitrogen ; LDH, lactic dehydrogenase

from antibiotic administration [59] A study of 74 patients with acute necrotizing pancreatitis treated with prophylactic imipe-nem demonstrated a signifi cantly decreased incidence of pancre-atic sepsis (12% vs 30%) [60] Similar results were observed by Sainio and colleagues [61] While further studies are needed to better defi ne both patient and antibiotic selection, antibiotic pro-phylaxis appears to be indicated in patients at high risk for septic complications such as pancreatic necrosis

Antienzyme and hormonal therapies have been designed to reduce the severity of disease by halting the production of pan-creatic enzymes and the subsequent cascade activation of the complement, kallikrein – kinin, fi brinolytic, and coagulation systems Studies evaluating atropine, calcitonin, glucagon, soma-tostatin, and the enzyme inhibitors, aprotinin and gabexate, however, have not shown improved morbidity or mortality in severe acute pancreatitis [4,26] Octreotide, a somatostatin ana-logue, has received considerable attention as a means to improve the course of acute pancreatitis Five randomized trials have been performed [62 – 66] which failed to demonstrate a clinical benefi t

Surgical t herapy

Although supportive measures are the mainstay of therapy, surgi-cal intervention also has a place in the management of acute pancreatitis The exact role, timing, and form of surgery remain

a matter of debate The one clear indication for surgery is for diagnosis of an acute abdomen An uncertain diagnosis mandates exploration for possible surgically correctable conditions Two other situations also may require surgery: gallstone pancreatitis and select anatomic or infectious complications

The goals of biliary surgery in cases of gallstone pancreatitis are

to prevent recurrence and to decrease morbidity and mortality

by removing the instigating agent Cholecystectomy and bile duct exploration are not performed, however, during the acute episode Because nearly 95% of stones pass during the fi rst week of illness, the utility of surgery early in the illness does not weigh heavily against the high mortality rates that have been reported for early biliary surgery [67] While not indicated in the acute phase of illness, biliary surgery should be performed after the acute pancreatitis subsides, prior to discharge from the hospital

An alternative to open surgical removal of bile duct stones has been developed utilizing ERCP Combined with endoscopic sphincterotomy, ERCP offers both diagnostic and therapeutic advantages in the critically ill patient [68,69] If performed within the fi rst 72 hours of illness, this procedure has been shown to decrease morbidity and length of hospital stay in patients with severe pancreatitis [69,70]

ERCP has been used in a number of pregnant patients without complications and has been found advantageous in the avoidance

of the potential risks of major surgery during pregnancy [71 – 76] ERCP during pregnancy is used to treat choledocholithiasis [69] Choledocholithiasis that causes cholangitis and pancreatitis during pregnancy increases the risk of morbidity and mortality for both the fetus and mother ERCP is safe during pregnancy

Management

Treatment of acute pancreatitis in pregnancy is similar to that of

non - pregnant individuals The initial treatment of acute

pancre-atitis is supportive medical management Because most cases are

mild and self - limiting, this approach is largely successful

Correction of any underlying predisposing factors, such as

avoid-ance or cessation of exacerbating factors like alcohol or drugs,

early endoscopic retrograde cholangiopancreatography (ERCP)

with obstructive jaundice, and reversal of hypercalcemia, is a

basic principle to be observed Assessment of prognostic

indica-tors, as discussed earlier, permits appropriate surveillance

Patients with more severe disease should be transferred to an

intensive care unit for continuous monitoring, because shock and

pulmonary failure can present early in the course of disease and

require prompt recognition and management

Medical therapy is comprised of fl uid and electrolyte

manage-ment, adequate analgesia, and elimination of oral intake

Intravenous fl uid resuscitation is a vital component of treatment

in both mild and severe cases Restoration of intravascular volume

and avoidance of hypotension is important for cardiovascular

stability and renal perfusion Electrolyte abnormalities are

common, including hypokalemia and metabolic alkalosis

from severe vomiting and hypocalcemia from fat saponifi cation

Serial assessment of electrolytes and appropriate replacement

are essential Parenteral analgesia is frequently necessary;

mor-phine compounds, however, should be avoided secondary to

their actions on the sphincter of Oddi Oral intake is withheld for

the duration of illness Most patients with mild pancreatitis

can be managed with intravenous fl uids In contrast, nutrition

should be implemented early in the hospital course of patients

with severe disease Enteral feeding may have advantages over

parenteral It has the potential benefi t of maintaining the

intesti-nal barrier (it is felt that bacterial translocation is probably the

major source of infection) Enteral nutrition also avoids catheter

related complications of parenteral nutrition such as line sepsis

[52,53]

Nasogastric suction may be appropriate in a subset of patients

with acute pancreatitis Nasogastric suction, however, does

not appear to infl uence duration of disease or its symptoms

Several studies have investigated the role of nasogastric suction

in mild to moderate pancreatitis and found no difference in

duration of abdominal pain, tenderness, nausea, and elevated

pancreatic enzymes or time to resumption of oral feeding

[54 – 56] Therefore, nasogastric suction should be utilized on an

elective basis for symptomatic relief for those patients with severe

emesis or ileus

Prophylactic antibiotics also have been advocated in an effort

to prevent the development of infectious complications Mild

cases of pancreatitis do not appear to benefi t from antibiotic

prophylaxis, although studies are few [57,58] In contrast, severe

cases with pancreatic necrosis have a high rate (40%) of bacterial

contamination and represent a subset of patients that may benefi t

situations, however, merit special consideration in pregnancy: the treatment of biliary disease and hypertriglyceridemia

The management of biliary disease in pregnancy raises the issue

of timing of surgery On resolution of acute pancreatitis, chole-cystectomy is typically performed in a non - pregnant patient prior

to discharge from the hospital Some advocate continued conser-vative management in pregnancy to avoid operative complica-tions and fetal morbidity A high relapse rate (72%), however, is often encountered [5,82] For patients presenting in the fi rst tri-mester, this may be as high as 88% Surgical intervention decreases the incidence of relapse and the risk of systemic complications Several studies support the use of second - trimester cholecys-tectomy for cholecystitis or pancreatitis [1,3,5,83,84] The second trimester appears optimal in order to avoid medication effect on organogenesis and a possible increased rate of spontaneous abor-tion in the fi rst trimester [1,3,5,83,84] Third - trimester patients are best managed conservatively because they are close to the postpartum period when operative risks are reduced Cholecystectomy may be performed by laparotomy or open lapa-roscopy The open technique for the laparoscopic approach is often best, in order to avoid puncture of the gravid uterus with blind trocar insertion

Fetal loss following cholecystectomy was once reported to be

as high as 15% [85] Many earlier reports, however, included patients undergoing surgery in the fi rst trimester suffering spon-taneous abortion many weeks postoperatively Because at least 15% of all pregnancies are now known to end in spontaneous abortion, and preterm labor is seen in up to 10% of all continuing pregnancies, it would appear that the actual rate of complications related to surgery probably approaches nil, a fi gure confi rmed by several recent studies [5,86,87] A review of studies from 1963 to

1987, evaluating fetal loss in patients undergoing cholecystec-tomy, revealed an 8% spontaneous abortion rate and an 8% rate

of premature labor [86] In a similar manner, laparoscopic cho-lecystectomy in the second trimester has been reported in a small number of patients, with no increase in fetal or maternal morbid-ity or mortalmorbid-ity [88,89]

Treatment of hypertriglyceridemia in pregnancy is aimed pri-marily at prevention of pancreatitis Fats should be limited to fewer than 20 g/day This restrictive diet, however, is not palatable and is diffi cult for patients to maintain Sanderson and associates [90] reported successful management of hypertrigliceridemia during an episode of pancreatitis and the remainder of gestation

by utilizing intravenous fl uid therapy to provide calories in the form of 5% dextrose and restricting oral intake to clear liquids Total parenteral nutrition offers another therapeutic approach when dietary adjustments are inadequate to prevent excessive triglyceride elevations Plasma exchange and immunospecifi c apheresis also have been investigated and have suggested that long - term extracorporeal elimination of lipoproteins may offer a safe and effective method of prevention and treatment of hyper-triglyceridemic pancreatitis in pregnancy [91] Fish oil supple-ment ( > 3 g/day) can also be quite effective in lowering triglycerides [92,93]

and may be performed with modifi ed techniques to reduce

radia-tion exposure to the fetus and without fl uoroscopy [75,76] If

there is radiation exposure during ERCP, the dosimetry should

be routinely recorded

Surgery for early and late complications of pancreatitis has also

been the subject of controversy A few situations appear to be

clear indications for surgical intervention, such as acute, life

threatening hemorrhage However, the timing and type of

surgi-cal procedures for later complications, such as sterile necrosis,

pseudocyst, and abscess, are less straightforward Using the

devel-opment or persistence of organ failure despite 72 hours of

inten-sive medical therapy as indications for surgery, Gotzinger and

colleagues [77] reported on 340 patients who underwent surgical

exploration for acute pancreatitis Control of pancreatic necrosis

(total removal of necrotic tissue) was accomplished in 73% of

patients, requiring an average of 2.1 operations Mortality was

100% in patients in whom surgical control of necrosis could not

be accomplished versus 19% in those patients who did achieve

surgical control of necrosis

Arterial hemorrhage occurs in 2% of patients with severe

pan-creatitis Necrosis and erosion into surrounding arteries of the

gastrointestinal tract result in massive intra - abdominal or

retro-peritoneal hemorrhage Arteriographic embolization followed by

surgical debridement and artery ligation improved survival from

0% to 40% [78] In contrast, the development of sterile pancreatic

necrosis is not an automatic indication for surgery, because up to

70% of cases will resolve spontaneously While few studies have

been performed, no benefi t for early debridement has been

dem-onstrated [79,80]

The formation of pseudocysts may mandate surgical

debride-ment based on clinical characteristics Occurring in as many as

10 – 20% of patients with severe acute pancreatitis, pseudocysts

resolve in approximately 50% of cases [26] Surgery is performed

if symptoms of hemorrhage, infection, or compression develop

or if the pseudocyst exceeds 5 – cm or persists longer than

6 weeks Internal drainage represents the superior surgical

approach, although percutaneous drainage may temporize a

criti-cally ill patient Fluid should be collected for culture to rule out

infection

Finally, pancreatic abscess formation occurs in 2 – 4% of

patients with severe pancreatitis and is 100% lethal if left

und-rained Although percutaneous drainage may be temporizing, the

catheter often becomes occluded secondary to the thick purulent

effl uent With early and aggressive surgical debridement,

mortal-ity is reduced to 5% [81] Either transperitoneal or

retroperito-neal approaches may be appropriate Postoperatively, 20% will

require reoperation for incomplete drainage, ongoing infection,

fi stulas, or hemorrhage [81]

Considerations in p regnancy

Treatment of pancreatitis does not differ in the pregnant patient

Supportive measures are identical to those of the non - pregnant

patient, and severe complications are managed aggressively Two

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Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,

M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd.

Shad H Deering 1 & Gail L Seiken 2

1 Department of Obstetrics and Gynecology, Uniformed Services University of Health Sciences, Old Madigan Army Medical Center, Tacoma, WA, USA

2 Washington Nephrology Associates, Bethesda, MD, USA

Introduction

Renal failure is now an uncommon complication of pregnancy

in developed countries, occurring in less than 1% of all

pregnan-cies in developing countries, although specifi c diagnostic criteria

have not always been well defi ned in the literature [1,2] In fact,

the incidence of acute renal failure (ARF) requiring dialysis is

now not signifi cantly different in pregnant women in Western

countries compared with the worldwide population One large

analysis reported that the incidence of ARF in pregnancy fell from

1 in 3000 to 1 in 18 000 between the years 1958 and 1994 [3] In

previous decades, rates of ARF as high as 20 – 40% were reported

in pregnancy, largely attributed to the high incidence of septic

abortion [4 – 6] When ARF does occur in underdeveloped parts

of the world, it is often secondary to limited prenatal/delivery care

and illegal abortion

As the incidence of pregnancy - related ARF in developed

coun-tries has sharply declined and treatment has improved, so have

maternal mortality rates reported in most studies This

improve-ment is related to both earlier recognition and intervention, as

well as availability of dialytic support Stratta et al reported no

deaths over the last 7 years of their experience, as compared with

previously reported rates as high as 31% [3] This is in sharp

contrast, however, to another study at an inner city hospital in

Georgia from 1986 to 1996 which documented 15% maternal and

43% perinatal mortality rates, respectively, as well as data from

India that suggest ARF in pregnancy may have a mortality rate as

high as 50% [7] These studies suggest that ARF in pregnancy

remains a potentially devastating complication

Etiologies of a cute r enal f ailure

The approach to the pregnant patient with ARF is similar to that

of the non - pregnant patient, although diseases unique to

preg-nancy (Table 28.1 ) must be considered in the differential diagno-sis [8] Disorders causing ARF in pregnancy include prerenal azotemia, intrinsic renal disease, urinary obstruction, as well

as pre - eclampsia, HELLP syndrome ( h emolysis, e levated l iver

enzymes, l ow p latelets), acute fatty liver of pregnancy (AFLP),

and postpartum renal failure, also known as postpartum hemo-lytic uremic syndrome (HUS) Bilateral renal cortical necrosis (BRCN) is another consideration in the evaluation of the preg-nant women with ARF, which, though not unique to the pregpreg-nant state, is seen overwhelmingly in pregnancy

In the past, a bimodal incidence of ARF was seen in preg-nancy, with a peak in the fi rst trimester corresponding to the high incidence of septic abortion, and a second peak in the third trimester corresponding to a number of other disorders seen uniquely in pregnancy Currently, with the decrease in the number of septic abortions, the majority of ARF is now seen in the latter part of gestation Additionally, accelerated loss of renal function, along with more diffi cult to control hyperten-sion and increased proteinuria, is seen in 10% of women enter-ing pregnancy with underlyenter-ing moderate to severe renal insuffi ciency due to a variety of causes [9] Although less common, signifi cant deterioration in renal function may also occur during pregnancy in women with underlying diabetic nephropathy [10]

Renal biopsy is infrequently performed during pregnancy as the clinical presentation and timing of renal failure is usually adequate to establish a diagnosis A renal biopsy may be indi-cated in pregnancy if there is a sudden deterioration of renal function without a defi nite cause before 32 weeks of gestation, especially if a diagnosis of pre - eclampsia is in doubt and a pre-mature delivery may be avoided by the information obtained

A large retrospective study of over 1000 percutaneous renal biopsies performed during pregnancy between 1970 and 1996 reported a complication rate of 2.4% [11] Another recent but smaller study of 18 renal biopsies performed in pregnancy and the early postpartum period reported a 38% incidence of renal hematoma, with nearly one - third of those affected requiring a blood transfusion [12] Because of advances in neonatal inten-sive care and the favorable long - term prognosis for infants born after 32 weeks of gestation, renal biopsy is generally not

period secondary to lacerations, uterine atony, or retained prod-ucts of conception Hemorrhage with resultant hypotension was

a major cause of pregnancy - associated ARF in 7% of patients studied at the Necker Hospital, and was a contributing factor in

as many as 79% of cases in other studies [1] A more recent study implicated postpartum hemorrhage in nearly 10% of ARF cases, and placental abruption in another 4% [7]

Patients with pre - eclampsia may be particularly susceptible to ARF associated with hemorrhage due to pre - existing alterations

in maternal physiology, including decreased intravascular volume, heightened vascular responsiveness to catecholamines and angiotensin II, and altered prostaglandin synthesis [14] In a study of 31 patients with pre - eclampsia and acute renal failure, Sibai and colleagues reported that 90% had experienced some form of signifi cant hemorrhage [15]

Intrinsic r enal d isease

Acute renal failure may result from a variety of intrinsic renal diseases similar to those in the non - pregnant patient Involvement

of the glomeruli may predominate in one of the many primary

or secondary glomerulonephritides The renal tubules and inter-stitium are the primary areas of injury in acute tubular necrosis (ATN) and acute interstitial nephritis (AIN) Both clinical pre-sentation and examination of the urinary sediment can provide valuable clues to the diagnosis, although renal biopsy may even-tually be required to distinguish among the many glomerular diseases and to predict prognosis (Table 28.3 )

Acute g lomerulonephritis

The numerous causes of acute glomerulonephritis (GN) include primary glomerular disease such as poststreptococcal GN, mem-branoproliferative GN, idiopathic rapidly progressive (or cres-centic) GN (RPGN), as well as secondary glomerular diseases such as lupus nephritis, systemic vasculitis, and bacterial endo-carditis (Table 28.4 )

The classic presentation of acute GN is that of hypertension, edema and volume overload, nephrotic range proteinuria, and an active urinary sediment with red blood cell casts (Table 28.3 ) In

performed after this gestational age as prolongation of

preg-nancy is less of a concern

Prerenal a zotemia

Prerenal azotemia is the result of decreased renal perfusion, due

to either true intravascular volume depletion, decreased cardiac

output, or altered renal perfusion The latter can be seen with

cirrhosis, nephrotic syndrome, renal artery stenosis, or the use

of non - steroidal anti - infl ammatory agents By defi nition,

prerenal azotemia is readily reversible with restoration of renal

perfusion

Early in pregnancy, hyperemesis gravidarum is one of the more

common causes of ARF secondary to profound volume depletion

resulting from poor oral intake and vomiting Similarly, any

gas-trointestinal illness with vomiting or diarrhea, excessive use of

cathartics or laxatives, or bulimia may result in prerenal

azote-mia Generally, these disorders are readily apparent on the basis

of history and laboratory fi ndings However, eating disorders,

which occur in up to 1% of pregnancies, are often diffi cult to

diagnose and require a high index of suspicion [13] To prevent

the development of fi xed renal tubular injury, prerenal azotemia,

due to hemorrhage or other causes, must be treated aggressively

with blood product support and fl uid resuscitation

Laboratory studies that may be of benefi t in establishing the

diagnosis of prerenal azotemia include urinary electrolytes and

osmolality (Table 28.2 ) The urine sodium is typically low, as is

the fractional excretion of sodium [(urine Na + /serum Na + )/

(urine creatinine/serum creatinine) × 100%], refl ecting a sodium

avid state, and urine osmolality is high, indicating intact urine

concentrating ability A low urine chloride may also provide a

clue to surreptitious vomiting

Uterine hemorrhage is an important cause of hypovolemia and

subsequent prerenal azotemia late in pregnancy Although usually

presenting as profuse vaginal bleeding, hemorrhage from

placen-tal abruption may be concealed or may occur in the postpartum

Table 28.1 Differential diagnosis of acute renal failure in pregnancy

Prerenal azotemia

Acute tubular necrosis

Acute interstitial nephritis

Acute glomerulonephritis

Obstruction

Pre - eclampsia *

HELLP syndrome *

Acute fatty liver of pregnancy *

Postpartum renal failure

Pyelonephritis

Bilateral renal cortical necrosis

* These occur almost exclusively after 20 weeks gestation, and mostly in the

third trimester of pregnancy

Table 28.2 Laboratory evaluation of acute renal failure

azotemia

Acute tubular necrosis

BUN: creatinine ratio > 20 : 1 10 : 1 Urine Na + (mEq/L) < 20 > 40 Fractional excretion of Na + (FENa + ) < 1% > 2%

Urine osmolality (mosm/kg H 2 O) > 500 < 350 Urine sp gr > 1.020 1.010 Urine sediment Bland Granular casts, renal

tubular epithelial cells

is usually avoided in pregnancy, it may be encountered in the case

of an intentional overdose Antibiotics such as the penicillins and

β - lactam antibiotics, and H 2 blockers are, however, used rou-tinely in pregnancy

Acute interstitial nephritis may also occur in association with viral infections, including cytomegalovirus and infectious mono-nucleosis, direct bacterial invasion, parasitic infections such as malaria and leptospirosis, and systemic diseases such as SLE and sarcoidosis (Table 28.5 ) Unlike acute GN, acute interstitial nephritis typically presents with modest proteinuria ( < 2 g/day), pyuria, eosinophiluria, hematuria, and white blood cell casts

on urinalysis Systemic manifestations may include fever, rash, arthralgias, and other signs of a hypersensitivity reaction in those patients with drug - induced interstitial nephritis Hypertension and edema are infrequently seen with AIN, except in those cases

of severe renal failure Withdrawal of the offending agent or treat-ment of the underlying infection or disease usually results in improvement of renal function In some cases of drug - induced

or idiopathic AIN, steroids have been used with varying degrees

of success When history, physical examination, and laboratory evaluation are inadequate to establish a diagnosis, renal biopsy may be necessary

Acute t ubular n ecrosis

Acute tubular necrosis may result from a variety of toxic expo-sures, including aminoglycosides, radiographic contrast, heavy metals, and several chemotherapeutic agents Pigment - induced

those women with pre - existing renal disease, these features are

often noted in the fi rst two trimesters of gestation, although

systemic lupus erythematosus (SLE) may manifest at any time

during pregnancy Laboratory analysis including serum

comple-ment levels, antinuclear antibodies, antistreptolysin - O titers,

antineutrophil cytoplasmic antibodies, and other autoantibodies

may be helpful in establishing a diagnosis, although in most cases

renal biopsy is eventually necessary Pre - eclampsia may mimic

acute glomerulonephritis in presentation, although serologic

evaluation should be negative It is important to attempt to

dif-ferentiate between the two in order to avoid delivery at a very

early gestational age as may be required for severe pre - eclampsia

Treatment of acute GN is largely supportive, including diuretics,

antihypertensive agents, and occasionally dialysis Depending on

the underlying disease, corticosteroids or cytotoxic agents may be

employed as well

Acute i nterstitial n ephritis ( AIN )

The most common cause of AIN is drug exposure and an

exten-sive list of agents have been implicated Among those more

com-monly noted are the β - lactam antibiotics such as the semisynthetic

penicillins, sulfa - based drugs, histamine H 2 blockers, and non

steroidal anti - infl ammatory agents (NSAIDs) While NSAID use

Table 28.3 Acute renal failure: evaluation of intrinsic renal disease

Urine sediment Brown granular casts Hematuria, pyuria, eosinophils, WBC casts Hematuria, renal tubular cells RBC casts, oval fat bodies Proteinuria < 2 g/day < 2 g/day > 2 g/day, possible nephrotic syndrome

FENa + > 2% > 2% < 1%

Systemic manifestations Hypotension, sepsis, hemorrhage Fever, skin rash, new medication Collagen - vascular disease, infection

Table 28.4 Causes of glomerulonephritis

Primary

Minimal change disease

Focal segmental glomerulosclerosis

IgA nephropathy

Membranoproliferative glomerulonephritis

Membranous nephropathy

Poststreptococcal glomerulonephritis

Secondary

SLE

Henoch – Sch ö nlein purpura

Cryoglobulinemia

Polyarteritis nodosa

Wegener ’ s granulomatosis

Hypersensitivity vasculitis

Goodpasture ’ s syndrome

Infection - related (i.e shunt nephritis, endocarditis)

Table 28.5 Causes of acute interstitial nephritis

Drug - induced Infection Viral: cytomegalovirus, infectious mononucleosis, hemorrhagic fever Bacterial: streptococcal infections, diphtheria, Legionnaires ’ disease Parasitic: malaria, leptospirosis, toxoplasmosis

Systemic disease Sarcoidosis Systemic lupus erythematosus

Sj ö gren ’ s syndrome Transplant rejection Leukemic or lymphomatous infi ltration Idiopathic