van Ruler O, Lamme B, Gouma DJ, et al. Variables associated with positive \201 ndings at relaparotomy in patients with secondary peri- tonitis. Crit Care Med 2007; 35: 468 \200\223 76. 514 S MUDAN The medical patient with surgical problems mentation should be avoided as it may cause bacteraemia, hemorrhage or perforation. CT exam ination is most help- ful in the diagnosis, and shows large bowel dilatation, bowel wall th ickening and sometimes pneumotosis. Any part of the colon can be involved, but more typical ly the right colon and terminal ileum. Treatment is supportive with \202 u- ids and antib iosis, and surgery is rarely helpful. Early intro- duction of G-CSF to hasten haemopoietic cell recovery can be helpful. The patient may progress slowly to a palpa- ble mass, but som etimes rapidly to a picture of sepsis and MOF. The differential diagnosis in these patients is usually between Clostridium dif \201 cile and CMV colitis. Rare causes of abdominal pa in such as porphyria cause great diagnostic dif \201 culty, and the nature of the disease is such that occasionally these will surface on the ITU per- haps masquerading as an acute epileptic \201 t. Spontaneous retroperitoneal haematoma in the anticoagu- lated patient i s a rare but potentially life-threatening event for the patient in the ITU. The initial eve nt is a fall in the hemoglobin, but compartment syndrome caused by the expansion of the hae matoma and complications thereof require radiological evaluation and sometimes interven- ti on. Radiological drainage is likely not to be effective, and open retroperitoneal drainage might be required. However, this tends to be a high morbidity procedure and potentially con taminates a sterile \201 eld, resulting in retroperitoneal abscess formation. In medical patients the incidence of a GI problem compli- cating an ITU admission is though t to be between 1 and 7%. This also applies to patients admitted following a non- abdominal major operation such as cardiac bypass or neu- rological surgery. The mortality hazard pre dicted by the admission severity risk scores is increased, and an abdomi- nal complication is a substantial contributor to ITU mortal- ity. Delays in diagnosis and surgical referral contribute to a deleterious outcome. High clinical suspicion and early reporting of abdomin al signs or unaccountable deteriora- tion in physiological parameters are fundamental to ma n- agement of the critically ill patient in the ITU. The background reason for admission, e .g. diabetic compli- cation, respiratory failure, cardiovascular disease or treat- ment-rel ated neutropenia, may determine the type of surgical problem that follows. Complications in clude GI bleed, perforation, cholecystitis, pancreatitis and intestinal ischaemia, the mort ality for the latter being close to 100%. Severe metabolic derangement such as uraemia and use of mechanical ventiliation and pressors quickly lead to erosive changes in the intestin al and gastric mucosa. Such patients are especially prone to GI hemorrhage and should have pharmacological prophylaxis. The bleeding is likely to be upper GI rather than lower GI, wi th a 2:1 ratio. Fresh red blood or blood clots passed rectally can be either a lower GI tra ct bleed or a brisk upper GI tract bleed. Melaena can only come from the upper GI tract (pr oximal to the liga- ment of Treitz) where the blood has been exposed to enzymic and acid ac tion. The patient should be resusci- tated, commenced on acid blockade and an upper GI endo scopy carried out. Bleeding from a gastric or duode- nal ulcer may be seen and treated via the endoscope by injection. A more \202 orid picture of a bleeding pan-gastritis is somet imes seen in the uraemic patient, and no local ther- apy is effective. For bleeding lesions not controlled by endoscopic means, the alternatives lie with surgery or with radiological embolization. The extensive blood supply of the stomach sometimes makes control of gastric bleeding by radiological embolization dif \201 cult. More dif \201 cult diag- noses such as gastro-oesophageal varices or a DieuLafoy abnormality obviously require the appropriate specialist input, as will unexpected \201 ndings such as a clinically occult cancer. Ble eding from the small intestine is very dif \201 cult to diagnose, and radiology by either CT or visceral angiogra- phy is often helpful here if it is active bleeding. Low volume ble eding might require deployment of wireless capsule endoscopy. Diverticular disease and the colitides cause bleeding from the colon, and the former usually presents with a substantial bleed of fresh blood that usually settles and does not re-bleed. Pancolitis tends to have a picture of small amounts of blood clot mixed with mucus, and is more dif \201 cult to se ttle. Colonoscopy should be considered and surgery for colectomy might be required. Neutrop enic colitis, a syndrome of non-speci \201 c nausea, abdominal swelling and pain, is seen 7 days after adminis- tration of cytotoxic chemotherapy. Bleeding is not a fea- ture. Feve r may be absent and blood count shows leucopenia and a neutrophil count typically below 1.5 \227 109/l. This problem is seen in patients having high dose chemotherapy such as for he matological malignancy, and is less common in chemotherapy for solid tumors. The chemistry shows a rising lactate and, in severe cases, liver and renal dysfunction. The colon is very soft, and instru- Obstructions Acute colonic pseudo-obstruction (Ogilvie \200\231s syndrome) is seen in the c hronically hospitalized or seriously ill patient. Spinal surgery and retroperitoneal bleedi ng or other space- occupying lesions are recognized causes. The syndrome consists of massiv e colonic dilatation in the absence of a mechanical obstruction, and is probably due to aut onomic failure. The abdomen is distended and bowel sounds are tinkling. Imaging shows a mas sive dilatation of the colon with preservation of haustral markings and a thin wall, in con tra- distinction from dilatation of colitis. Unprepared enema with gastrograffin should be carried out to rule out a mechanical problem and is on its own sometimes therapeu- tic in r elieving the problem. Ischaemia or spontaneous per- forations occur in 3% of cases, and in these the mortality is 40%. Other causes of non-obstructed colonic dilatation such as C. dif \201 cile or CMV-related colitis should be excluded. Initial treatment consists of cor rection of electrolyte abnor- malities, nasogastric aspiration and prokinetic therapy with erythromycin or sometimes neostigmine. Serial plain AXR is used to follow the patient, and a failure to settle on con- servative therapies requires intervention; the patient should h ave decompression by colonoscopy. Repeat colonoscopy is required in some patients. Caecal d ilatation of >10cm car- ries a risk of perforation, and surgery might be required if decomp ressive colonoscopy has failed. True mechanical obstructions in the ITU patient are not com mon. Previously undetected pathology such as a bowel tumor or complications of existing dis ease such as diver- ticulitis or intestinal adhesions are the common causes. In the elderly patient, one should be aware of incarceration of hernia, and the groin and surgical wounds should be inspected carefully. After initial conservative treatment, the solution usually lies with surgical intervention, the exact nature of which 515 CHAPTER 30.4 The medical patient with surgical problems will depend on the site of obstruction. The more recent advent of colonic stents can avoid operation in some colon obstructions involving the left colon, but are more dif \201 cult to place in the more proximal colon. De \201 nitive surgical solution is usually required at some time. air can be seen in the gallbladder. Surgery is always required to salvage the situation. Intra-abdominal hypertension Primary raised IAP may occur because of an intra-abdomi- nal p athology or be secondary to a non-abdominal event such as a major burn injury. Elevation of the IAP has adverse effects on pulmonary, cardiovascular, renal, splanchnic and neurologic al physiology. The mortality varies from 10 to 60%. IAH can be said to exist when the norma l IAP of 7mm Hg is exceeded. A pressure >20mm Hg and with new organ failure is termed abdo minal compartment syndrome. An increase in abdominal pressure >15mm Hg reduces the pulmonar y capacity, functional residual capacity and volume. Hypoventilation and increased PVR lead to hypoxia, hypercapnia and increased ventilatory pressue. Similarly, reduction in venous return from compression of the IVC and portal vein results in a down and right shift of the Starling curve. Renal tamponade causes a reduction in renal blood \202 ow at 15mm Hg an d results in anuria at an IAP >30mm Hg. Reductions in the splanchnic blood \202 ow and re duction in liver and gut blood \202 ow contribute to mucosal acidosis and breakdown of ba cterial integrity. The increased intrathoracic and central venous pressure leads to rises i n the ICP. Intervention to relieve the pressure is required somewhere between an IAP of 20 and 25mm Hg. If intervention is early, the effects are reversible, but prolonged abdominal com- partment syndrome leads to irreversible MOF regardless of decompression. Decompression of the abdomen by laparostomy is carried out, and the open abdomen managed by covering wit h a clear non-adherent plastic sheet or by a vacuum dressing to aid collection of the exuda tes and promote tissue per- fusion. Fluid losses after decompression to an open abdo- men c an be great, and require careful monitoring. Ischaemia of the bowel A secondary ischaemic event such as mesenteric infarction by occlusi on of the visceral vessels as either a thrombotic or embolic event may occur. Cardiac, auto immune and oncological diagnoses predispose to this complication. Conditions that cause spl anchnic hypoperfusion such as mechanical ventilation or use of vasopressors may be com- pli cated by non-occlusive ischaemia. Erosions can be detected in ITU patients 24h from admissi on, suggesting that stress-related mucosal ischaemia is an early event. The mortality from ischaemic bowel complicating the ITU admission is high, 60 \200\22370%. The patient usuall y presents with intense pain which appears to be out of proportion to the clinical signs in the abdomen. The abdomen is often diffusely distended with a doughy feel. The lactate is e le- vated and rises progressively, the abdominal signs of peri- tonitis become more obvious and extensive necrosis is present, and usually by this stage the patient is extremely ill and beyond the point of surgical salvage. Early diagnosis is dif \201 cult. CT may be help ful in showing wall thickening, lack of enhancement in the bowel wall, pneumotosis and pos- sibly portal venous gas. Early surgical consultation should be sought. Failure to settle a nd a rising lactate should initi- ate further investigation by consideration of laparotomy or laparoscopy to examine the abdominal contents. In the past, we have favored bedside lapa roscopy, to avoid mov- ing a potentially unstable patient, and transfer to theater only for those few with ischaemic gut thought suitable for surgical salvage. Acalculous cholecystitis (ACC) ACC occurs with an incidence of 1% in the ITU patient. The e tiology may relate to end-organ perfusion. The clini- cal picture is of right upper quadran t pain and in \202 amma- tion. The initial management is with antibiotics and then surgery if there is a failure of rapid resolution. In the unsta- ble patient, percutaneous drainag e should be carried out. While cholecystitis can be seen on CT scan, interrogation of the b iliary system is often better with ultrasound and has the advantage of being available at t he ITU bedside, obviating transfer to the radiology department of a sick patient. Soft tissue infections Necrotizing fasciitis is a serious and potentially life-threat- enin g infection more common in the severely ill patient. Predisposing factors include, peripher al vascular disease, liver disease, renal disease, malignancy, immunocompro- mise, diabetes , perianal sepsis, chronic skin disease and skin trauma, even of a minor nature. Classi \201 cation is into three groups depending on the organisms involved. Type 1 results from a mixed aerobic and anaerobic \202 ora found in sites of surgical trauma and in the perine um, typically group A -haemolytic streptococci, S. aureus, E. coli, Bacteroides spp, Pseu domonas sp. and Clostridia spp. Type 2 is found typically in the extremities and ia infecte d with group A -haemo- lytic streptococci and S. aureus. Type 3 is asscociated with Vibri o vulni \201 cus and is caused by skin puncture from marine insects and \201 sh. Fournie r \200\231s gangrene is a particular type 1 necrotizing fasciitis affecting the perineum an d caused by perianal conditions or involving the genitourinary tract. Mortality can be 20 \200\22350%, and is greatest in the elderly, obese, diabetic or immunocompromised patients. The pathogenesis is by implantation of bacteria possibly from a remote site such as a Bart holin \200\231s cyst or an anocu- taneous \201 stula into the subcutaneous tissue. Subseq uent proliferation and release of bacterial toxins causes Gall stone ileus A rare cause of intestinal obstruction is a rare complication of a common enough condition. Gallstone ileus is occa- sionally seen in elderly patients. Following an attack of acute cholecystitis, a large (>2cm, <5cm) stone from within the gallbladder erode s through the gallbladder and into the adjacent gut (1% of cases of acute cholecystitis in the eld- erly), usually the duodenum, leaving a cholecystoduodenal \201 stula. Progess of the stone through the intestinal tract eventually leads to lodgement of the stone in the n arrow terminal ileum, classically 60cm from the ileocaecal valve, and small bowel obstructi on follows. Occasionally a very large stone may give rise to Bouvret \200\231s syndrome whe re the large stone lodges in the duodenum and causes a gastric outlet obstruction. Classica lly imaging reveals Rigler \200\231s triad of intestinal obstruction, ectopic gallstone and pneumobilia; sometimes 516 S MUDAN thrombosis of the microvasculature, lysis and necrosis of the subcutaneous tissues. The cli nical course is rapid and begins with painful oedema and erythema of the skin. There may be systemic distur- bance ranging from \202 u-like illness to toxic shock syndrome in rapid ly progressing patients. The local changes progress to bullae, and the skin color changes f rom red to purple and then black. Crepitations might be felt if gas-forming organisms are p resent. A fulminant case may show spread of necrosis over a matter of hours, and so repeate d clinical examination every few hours is essential. Early recognition and initiation of tr eatment is essential. IV antibiotics should be commenced. If necrosis is evident then aggre ssive surgical debridement will be required, often serially. If the patient survives, recon struction by tissue \202 aps or skin graft might be required. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from the International Conference o f Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommend ations. Intensive Care Med 2007; 33: 951 \200\22362. Chou JW, Hsu CH, Liao KF, et al. Gallstone ileus: report of two cases and review of the lit erature. World J Gastroenterol 2007; 13: 1295 \200\2238. De Waele JJ, Hoste EA, Malbrain ML. Decompressive laparotomy for abdominal compartment synd rome \200\224a critical analysis. Crit Care 2006; 10: R51. Edelman DA, Sugawa C. Lower gastrointestinal bleeding: a review. Surg Endosc 2007; 21: 514 \200\22320. Fazel A, Verne GN. New solutions to an old problem: acute colonic pseudo-obstruction. J Clin Gastroenterol 2005; 39: 17 \200\22320. Filsou \201 F, Rahmanian PB, Castillo JG, et al. Predictors and outcome of gastrointestina l complications in patients undergoing cardiac surgery. Ann Surg 2007; 246: 323 \200\2239. Masannat Y, Masannat Y, Shatnawei A. Gallstone ileus: a review. Mt Sinai J Med 2006; 73: 1132 \200\2234. Salcido RS. Necrotizing fasciitis: reviewing the causes and treatment Further reading Achyra PS, Lipson DA. Gastrointestinal complications of acute res- strategies. Adv Skin Wound Care 2007; 20: 288 \200\22393. Saunders MD. Acute colonic pseudo-obstruction. Gastrointest piratory failure. Clin PulmonMed 2003; 10: 80 \200\2234. Endosc Clin N Am 2007; 17: 341 \200\22360, vi \200\223vii. Anaya DA, Dellinger EP. Necrotizing soft-tissue infection: diagnosis Williams N, Scott AD. Neutropenic colitis: a continuing surgical and management. Clin Infect Dis 2007; 44: 705 \200\22310. challenge. Br J Surg 1997; 84: 1200 \200\2235. 517 Chapter 31 Obstetric emergencies Chapter contents Pre-eclampsia 518 Eclampsia 520 HELLP syndrome 522 Postpartum hemorrhage 524 Amniotic \202 uid embolism 526 518 M DRESNER Pre-eclampsia Pre-eclampsia is a common complication of pregnancy, UK incidence is 3 \200\2235%, with a c omplex hereditary, immunologi- cal and environmental etiology. Special investigations \200 Hematology. Pre-eclampsia induces a hypercoagulable state, but can also cause thrombocytopa enia and coagu- lopathy. In mild disease, the FBC is normal. A platelet count <100 x 109/l is an indicator of severe disease, and should trigger full coagulation studies. The rate of decline of platelet count is more important than the absolute \201 gure, with a rapid de cline indicating aggressive disease. If anemia is noted, tests for haemolysis should be per - formed and HELLP syndrome excluded. Biochemistry. GFR and renal perfusion both decline in pre-eclampsia, and mild elevations in urea and creatinine may be seen, but serious renal d ysfunction is rare unless a second insult occurs, such as hemorrhage. If oliguric, it is im portant to monitor biochemistry, especially serum potassium. Obstetricians traditionally mo nitor serum urate levels as a marker of disease severity, but this is of no therapeutic rel evance for anesthetists. LFTs should be monitored for signs of HELLP syndrome. Radiology. R arely indicated, but a CXR may be necessary if pulmonary oedema is suspected through hypoxi a or crepitations. Neurological deficit after convulsions should raise the suspicion of cer ebral hemorrhage. If a patient is intubated and ventilated after a convulsion, return of no rmal neurology cannot be clinically con- \201 rmed and CT scanning should be considered. Fetal studies. Cardiotocography, fetal growth, liquor vol- ume and umbilical artery Doppler studies are all used to monitor fetal well-being. These will determine fetal indi- cations for early delivery. Pathophysiology Abnormal placentation is characterized by impaired myo- metrial spiral arte ry relaxation, failure of trophoblastic invasion of these arterial walls and blockage of so me ves- sels with \201 brin, platelets and lipid-laden macrophages. There is a 30 \200 \22340%, reduction in placental perfusion by the uterine arcuate arteries as seen by Dopple r studies at 18 \200\22324 weeks gestation. Ultimately the shrunken, calci \201 ed, and mi croembolized placenta typical of the disease is seen. The placental lesion is responsible f or fetal growth retarda- tion and increased risks of premature labor, abruption and fetal d emise. Maternal systemic features of this condi- tion are characterized by widespread endot helial damage, affecting the peripheral, renal, hepatic, cerebral, and pul- monary vasculat ures. These manifest clinically as hyperten- sion, proteinuria and peripheral oedema, and i n severe cases as eclamptic convulsions, cerebral hemorrhage (the most common cause of deat h due to pre-eclampsia in the UK), pulmonary oedema, hepatic infarcts and haemor- rhage, co agulopathy and renal dysfunction. Risk factors include: 1 positive family history 2 pre-ecl ampsia in a previous pregnancy with the same partner 3 conditions associated with large placental mass, includ- ing obesity, diabetes, multiple pregnancy and hydatidi- form mole. Management Mild disease does not require speci \201 c treatment, but the mother and fetus should be regularly monitored for signs of severe disease. If there are signs of severe dis ease, the patient should be monitored in a high dependency setting with regular, 15min, blo od pressure measurement till stabi- lized and then hourly. Fluid balance should be meticulo usly recorded, with urine output measured with an in-dwelling catheter. Proteinuria should be assessed hourly. Continuous oxygen saturation and hourly respiratory rate should be inst ituted to monitor for signs of pulmonary oedema. Central venous and pulmonary artery pressu re monitoring are not required except possibly after signi \201 cant haemor- rhage, persis tent pulmonary oedema or during ventilation on intensive care. Speci \201 c therapies incl ude the following. Severe pre-eclampsia is de \201 ned by the degree of hyperten- sion and proteinuria, and b y the presence of epigastric pain, headache, visual disturbance, severe oliguria, convulsio ns, pulmonary oedema and HELLP syndrome. Precise criteria for severe pre-eclampsia vary bet ween units, but most are based on the de \201 nitions of Davey and MacGillivray. Those sho wn below are used in the Yorkshire Pre-eclampsia pro- tocol, and are widely accepted. Clinical features Rare before 20 weeks gestation, but early onset indicates poor prognosis. It is more common in young women, prim- iparas and women of poor socioeconomic background. It is vital to identify severe disease (mild disease does not indi- cate speci \201 c tre atment), and failure to monitor adequately or to appreciate the signi \201 cance of the sy mptoms of severe disease are consistent features of substandard care with its consequences. Antihypertensive therapy The immediate goal is to treat extremes of systolic pres- sure, si nce it is most likely that shearing forces during sys- tole are the precipitant for cerebra l hemorrhage. There is no clear safe maximum pressure, but 160mm Hg has been suggested. The re is also no clear evidence indicating the best antihypertensive regimen, and local famili arity and experience is probably more important than which drug is used. One example regime n is: \200 History and examination: key points Diagnostic criteria of severe preeclampsia are: \200 \200 Eclampsia Severe hypertension. SBP >170mm Hg or DBP >110mm Hg from 3 readings over 15min, w ith at least 1+ of pro- teinuria. Moderate hypertension. SBP >140mm Hg or DBP >90mm Hg from 3 readings over 45min, with at least 2+ of proteinuria. Plus any of the following: headach e, epigastric pain, visual disturbance, clonus, papilloedema, liver tenderness, platelets < 100 x 109/l, ALT >50IU/l. Labetolol is a suitable \201 rst-line therapy, beginning with the oral route if tolerated . Initial administration of two doses of 200mg 1h apart is often effective. If not, or if t he oral route cannot be tolerated, IV therapy should be instituted with a bolus of 50mg ove r 1min, repeated as necessary to a maximum of 200mg. This should be followed with a continu ous infusion of 20 \200\223160mg/h as required. 519 CHAPTER 31.1 Pre-eclampsia If labetolol cannot be tolerated because of asthma or bradycardia, or if labetolol has fail ed to control the hypertension, nifedipine 10mg 6 hourly is a suitable sec- ond-line agent. Ventilated patients will bene \201 t from the hypotensive effects of sedative agents, som etimes obviating the need for speci \201 c hypotensive therapy. Rebound hypertension shoul d be anticipated and prevented during weaning. rapidly. In this situation, magnesium should be stopped until the urine output is restored. If signs of toxicity occur (loss of re \202 exes, respiratory weakness, dysrrhythmia), th e anti- dote to magnesium is 10ml of calcium gluconate. Thromboprophylaxis Because of the hypercoaguable state induced by pre-eclamp- sia, LMWH, e. g. 40mg clexane, should be administered daily. Appropriate timing of regional anesthesia an d removal of epidural catheters must therefore be born in mind. Fluid management Here is the key: oliguria in pre-eclampsia can be due to volume depletion (pre-renal), glomerular capillary endotheliosis (renal) or a combination of the two. In the absence of a secondary pre-renal insult such as haemor- rhage, the renal lesion is complet ely reversible and is not incipient acute tubular necrosis. In addition to this, severe pre -eclampsia damages the pulmonary capillary endothe- lium, lowering the pressure threshold f or pulmonary oedema. These points mean that aggressive \202 uid therapy is both unnecessa ry and dangerous. Indeed, it is not long since pulmonary oedema (with a signi \201 cant ia trogenic component) was the leading cause of death in pre-eclampsia in the UK Women with se vere pre-eclampsia in Yorkshire receive 80ml/h total fluids (plus replacement of extra loss es through bleeding, vomiting, etc.) and a urine output of down to 80ml over 4h is tolerate d. Cautious \202 uid chal- lenges are used, and in some cases diuretics are used to resto re urine output. This approach is contrary to the typi- cal management of critical care pat ients with multi-system disease, but has reduced the incidence of pulmonary oedema and crit ical care admissions, without any concur- rent rise in renal problems. However, few data or experi- ence exist regarding fluid management in ventilated pre-eclamptic patients. If sho uld be born in mind that if higher vascular \201 lling pressures are used to improve rena l perfusion during IPPV, pulmonary oedema can occur after extubation. In summary, the venti lated patient should have cautious \202 uid management, and typical critical care targets for CVP and urine output should be not be used. Timing and mode of delivery The only indication for immediate delivery is severe fetal dist ress or abruption. In the presence of maternal indica- tions for early delivery, such as se vere hypertension or eclamptic convulsion, it is desirable to stabilize the woman \200\231s condition before delivery with antihypertensive therapy and magnesium. This may also allow enough time for steroids to be administered to assist fetal lung matura- tion. Before 32 w eeks gestation, Cesarean delivery is indi- cated, but after 34 weeks vaginal delivery is co nsidered. After delivery, uterotonic agents containing ergometrine should not be used, as t hese can exacerbate hypertension. Anesthetic care Once coagulopathy has been excluded, regional analgesia and anesthesia are appropriate techniques. Fluid preload- ing is inappropriate because of the risk of relative hyper- volaemia and pulmonary oedema as regional blockade recedes. Pre-eclamptic women are resistant to the hypo- tensive effects of regional anesthesia, so spinal anesthesia is saf e and vasoconstrictor requirements are usually reduced. If general anesthesia or intubation are required, steps to prevent pressor responses should be employed. Bolus alfentanil of r emifentanil infusion are suitable tech- niques. Post-operative recovery should take place i n a high dependency setting. Further reading Clark VA, Sharwood-Smith GH, Stewart AVG. Ephedine requirements are reduced during spinal anesthesia for cesarean section in preeclampsia. Int J Obstet Anesth 2005; 1 4: 9-13. Davey DA, MacGillivray I. The classi \201 cation and de \201 nition of hyper- tensive dis orders of pregnancy. Am J Obstet Gynecol 1988; 158: 892 \200\2238. Magnesium sulfate therapy This should be considered for all women with severe pre- eclampsi a as prophylaxis against eclampsia. It should be delivered as a loading dose, followed by a n infusion for 24h, or until 24h after delivery, whichever comes \201 rst. The regi- men consists of: \200 \200 As deep tendon re \202 exes are abolished before magnesium leve ls reach cardiotoxic levels, blood level monitoring is not necessary with this regimen unle ss a patient is para- lysed. If urine output falls below 100ml in 4h, levels can rise Duley L, Hendrson-Smart DJ, Meher S. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev 2006; (3): CD001449. Magpie Collaborative Group. Do women with pre-eclampsia and their babies bene \201 t from magnesium sulfate? Lancet 2002; 359: 1877 \200\22390. Loading dose of 5g over 25min Continuous infusion of 1g/h Why Mothers Die 2000 \200\2232002. Report on con \201 dential enquiries into maternal deat hs in the United Kingdom. www.cemach.org.uk Why Mothers Die 1994 \200\2231996. Report on co n \201 dential enquiries into maternal deaths in the United Kingdom. www.cemach.org.uk 520 M DRESNER Eclampsia Management of eclampsia General \200 \200 \200 Eclampsia is seizure activity in a pregnant or peripartum woman with pre-eclampsia, where n o evidence of other cerebral conditions exists. It is more common in devel- oping nations. UK incidence is 1 case per 2500 materni- ties, with a mortality of 1.8% (survey, performed by the British Eclampsia Survey Team), i.e. 1 \200\2232% of women with pre-eclampsia. Proph ylactic magnesium sulfate therapy has become standard practice in severe pre-eclampsia, so the incidence of eclampsia may have fallen in the UK, but as 41% of cases of eclampsia in t he survey presented before the diagnosis of pre-eclampsia had been made, magnesium prophyla xis will never abolish eclampsia completely. The pathophysiology of eclamptic convulsions i s unclear. Ischaemia, hemorrhage, infarct and oedema have all been identi \201 ed by imagi ng and autopsy, and cerebrovascular endothelial damage is postulated to be the underlying p a- thology. The hydrostatic effects of hypertension may play a part, but many victims of ec lampsia have only moderate hypertension before convulsing. Teenage women are 3 times more l ikely to suffer eclamp- sia than their older counterparts, and multiple pregnancy increases the risk 6-fold. maintenance of a clear airway ensuring adequate oxygenation protection against aspiration Magnesium sufate; loading dose 4 \200\2236g over 20min amd infu- sion at 1 \200\2233g/h. Te rminating convulsions. Most eclamptic convulsions last <2min and are followed by a typical post-ictal phase, during which normal gross neurology can be con \201 rmed, allaying fears of cerebral hemorrhage. Avoid general anesthesia, where possible. Good conservative airway management in a lateral position and oxygen via face mask whilst await- ing rapid spontane ous resolution of the convulsion is ideal. Sedation and paralysis, which may be necessary, preclude this assessment, forcing clinicians to use imaging to exclude cerebral hemorrhage. Anticonvulsant therapy Magnesium sulfate is the most effective and safe therapy for eclamps ia. Its role in reducing the incidence of re-con- vulsion is clear, but its value as an acu te anticonvulsant is debatable. Most eclamptic convulsions have stopped spon- taneously bef ore the magnesium loading dose is given. In the presence of persistent or multiple convulsi ons, it is rea- sonable to add an easily titrated benzodiazepine such as midazolam. A secon d \201 t despite magnesium should prompt an increase of the infusion to 1.5g/h. If \201 ts still persist or the airway and oxygenation cannot be adequately maintained, intubation and ventilation are justi \201 ed. Clinical features Premonitory signs: headache, visual disturbance, followed by epigastric p ain. Around 40% of cases will present without warning symptoms, and before hypertension and proteinu- ria are identi \201 ed. Presentation: Convulsions occur antenatally in 38%, int ra- partum in 18% and postnatally in 44%. In 12% of postna- tal cases, the convulsion occur red >48h after delivery. Convulsions usually last for 1 \200\2232min and are self-limiting, but a second convulsion can occur within minutes. Other therapies Antihypertensive agents and \202 uid management should be instituted as f or any woman with severe pre-eclampsia. Hematological and biochemical investigations should be performed to monitor for other features of severe pre- eclampsia and HELLP. Prior to de livery, fetal monitoring should be instituted immediately from the time of convul- sion to monitor for signs of fetal distress. History and examination Eclampsia can occur with no previous indicators of pre- eclampsia. After a convulsion, it is important to question relatives about any history of neurological disease and of the occurrence of symptoms of severe pre-eclampsia. Neurological examinatio n should be performed at the ear- liest opportunity to exclude signs of cerebral haemor- rh age, and regular monitoring for hypertension, proteinuria and pulmonary oedema should begin . Delivery Fetal distress is common during a convulsion, and this may necessitate immediate o perative delivery under general anesthesia. However, if the fetal condition is acceptable, it may be possible to institute magnesium and antihyperten- sive therapy before delivery. P latelet and coagulation tests should be performed before regional anesthesia is used. Special investigations \200 The same hematological and biochemical tests used in severe pre-eclampsia should be perform ed. Radiology. A CT scan may be indicated to exclude cere- bral hemorrhage. This should be suspected if focal neu- rological signs are found or if persistent unconsciousness follows a convulsion. Fetal studies. Continuous cardiotocography should be instituted in antenatal women. Further reading Douglas KA, Redman CWG. Eclampsia in the United Kingdom. BMJ 1994; 309: 1395 \200\223400. Duly L. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative ecla mpsia trial. Lancet 1995; 345: 1455 \200\22363. This page intentionally left blank 522 M DRESNER HELLP syndrome should be anticipated, and in advanced pregnancy it is advisable to proceed to early delive ry before serious coag- ulopathy develops. In early pregnancy, risks to the neonate are obv iously much increased by delivery, so sympathetic counseling is vital for both partners. HELLP stands for Haemolysis, Elevated Liver enzymes, and Low Platelets, and is a severe var iant of pre-eclampsia peculiar to humans. It occurs in 20% of cases of severe pre-eclampsi a, with a mortality of 1 \200\2233.5%. Its insidious presentation and potential for sudden exacerbation fre- quently catches clinicians unaware, and its management re- quires rapid, multidisciplinary input. 80% of cases present before term, but 1/3 of cases are identi \201 ed after delivery. Premature delivery contributes to the very high perinatal mortality associated with HELLP syndrome. Glucocorticosteroids Observations that glucocorticoids, given to stimulate mat- uration of the fetal lungs, were associated with improve- ment of some of the markers of HELLP syndrom e, led to several clinical trials and a Cochrane Review. Whilst no clear improvements in ma ternal and perinatal mortality were found, higher platelet count, reduced hospital stay and higher birth weight followed steroid therapy. Prednisolone has limited placental transfer, so for bene \201 ts to mother and fetus, dexamethasone or betamethasone should be used. Clinical features While only 10% of cases present before 27 weeks, most do so before 36 wee ks gestation. Symptoms and signs are common but non-speci \201 c, and do not \201 t the usual pattern of severe pre-eclampsia. In addition to this, hypertension and proteinuria ar e not necessarily severe. There is there- fore great potential for diagnostic delay while s imple malaise rapidly progresses to anemia, coagulopathy and hepatorenal failure. There is also considerable risk of iatro- genic problems, largely through \202 uid overload during the treatment of haemolysis, thrombocytopaenia, coagulopa- thy and hemorrhage. As a \201 nal insult, recovery after deliv- ery is much more protracted than simple pre-eclampsia, a nd indeed the condition may worsen for the \201 rst 48h. For example, women with a platel et count <50 x 109/l may take 11 days to achieve a count >100 x 109/l. Of all pre-eclamptic patients, HELLP syndrome women are the most likely to require critical care, including ren al sup- port and possibly ventilation. Fluid management Renal function is precarious, with the renal lesion of pre- eclampsia comp ounded by hepatic disease, third space losses and a high incidence of hemorrhage. However, pul- monary oedema is also commonly associated with HELLP. Careful \202 uid balance is th erefore essential, but it can be easily derailed by the combination of hematological de \201 - cits and hemorrhage. Fluid overload may necessitate early dialysis if pulmonary oede ma is to be averted, because the kidneys may not respond adequately to diuretics. In ante- natal women, pulmonary oedema can precipitate the need for urgent Cesarean delivery in the face of coagulopathy, and a spiral of decline from massive hemorrhage to multi- system fail ure. History and examination \200 Key points \200 Symptoms: malaise (90%), epigastric pain (90%), nausea and vomiting (50%), and \202 u-lik e symptoms. Signs: right upper quadrant tenderness (80%), weight gain and peripheral oedema (60%). Hypertension and proteinuria may be mild or even absent. Symptoms and signs are non-specific, so diagnosis depends on close attention and a low thre shold for fur- ther investigation. Anticipate and plan for exacerbation to hepatorenal fail - ure, hemorrhage and pulmonary oedema. The early input of senior hematology, critical care and renal support clinicians is vital. Special investigations There is disagreement over the speci \201 c hematological and bioch emical criteria for the diagnosis of HELLP, but trends are more important than absolute \201 gures. \200 Further reading Martin JN Jr, Blake PE, Lowry SI, et al. Pregnancy complicated by preeclamp sia \200\223eclampsia with the syndrome of hemolysis, ele- vated liver enzymes, and low pla telet count: How rapid is post- partum recovery? Obstet Gynecol 1990; 76: 737 \200\22341. Hematology. Haemolysis can be identi \201 ed with a blood smear, rising LDH and rising tot al bilirubin. A platelet count <100 x 109/l is an agreed diagnostic criterion of HELLP. As liver function deteriorates, coagulation tests will also become abnormal. All hematological problems can be exacerbated by hemorrhage and dilution with IV \202 uids. Biochemistry. The levels of AST and ALT used to de \201 ne raised liver enzymes vary widely between auth ors. Local laboratory normal values and trends should therefore be used. Serum albumin will also fall, especially in cases complicated by hemorrhage and multi-system failure. Matchaba P, Moodley J. Corticosteroids for HELLP syndrome in pregnancy. Cochrane Database S yst Rev 2004: (1): CD002076. Sibai BM, Mabie BC, Harvey CJ, et al. Pulmonary edema in sever e preeclampsia \200\223eclampsia: analysis of thirty-seven consecutive cases. Am J Obstet G ynecol 1987; 156: 1174 \200\2239. Sibai BM, Ramadan MK, Usta I, et al. Maternal morbidity and mortal- ity in 442 pregnancies with haemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). Am J Obstet Gy necol 1993; 169: 1000 \200\2236. Management General High dependency care and regular fetal monitoring are required once HELL P syndrome is diagnosed. Deterioration This page intentionally left blank 524 A PINDER & M DRESNER Postpartum hemorrhage