کتاب بیهوشی به زبان ساده تألیف دکتر حامد بیضایی

((کتاب بیهوشی به زبان ساده))

تألیف دکتر حامد بیضایی متخصص بیهوشی ومراقبتهای ویژه

منتشر شد

كتاب بيهوشي ميلر مرجعي كامل و معتبر در علم بيهوشي است. كتاب BASIC ميلر نيز به عنوان چكيده‌ای از مطالب آن جهت آشنايي همكاران و فراگيري سريع‌تر بيهوشي كمك بسيار مي‌نمايد. نحوه گفتار و پراكندگي مطالب اين كتاب آن چنان است كه گاه مانع درك صحيح و برداشت درست از آنچه بايد بدانيم، می‌شود.

ممكن است دانشجويان كارشناسي بيهوشي نيز كه از اين كتاب به عنوان مرجع استفاده می‌كنند، با همين مشكل مواجه گردند، لذا ارائه كتابي كه بتواند به راحتي مطالب را در اختيار گذارد، الزامي به نظر مي‌رسيد.

اين كتاب نكات برجسته پنجمين چاپ كتاب BASIC ميلر (چاپ سال 2007 ميلادي) را در بر داشته و حاصل تدريسي است كه در كلاس‌هاي دانشجويان ارائه گرديده است.

براي فهم بهتر اين كتاب، از كتابهاي ديگري همچون Clinical Anesthesiology نوشته G. E. Morgan (چاپ چهارم - 2006 ميلادي)، Nurse Anesthesia Secrets نوشته Mary Karlet (چاپ اول - 2005 ميلادي) و Miller^'s Anesthesia نوشته Ronald D. Miller (چاپ هفتم – 2010 ميلادي) استفاده گرديده است.

كتاب حاضر براي تمامي افرادي كه در عرصه بيهوشي خدمت می‌نمايند، نوشته شده و در سه جلد ارائه خواهد شد.

جلد اول شامل 13 فصل بوده و مباحث زير را شامل می‌شود:

مقدمه‌ـ تاريخچه‌ـ داروها‌ـ اداره راه هوايي‌ـ بي حسي‌هاي رژيونال (نورآگزيال و محيطي).

در جلد دوم و سوم نيز مباحث زير گنجانده خواهد شد:

فيزيولوژي قلب و ريه‌ـ سيستم اتونوم‌ـ ارزيابي قبل از عمل‌ـ انتخاب نوع بيهوشي‌ـ سيستم‌هاي بيهوشي‌ـ پوزيشن‌ها‌ـ مونيتورينگ‌ـ مايع درماني و ترانسفوزيون‌ـ بيماريهاي قلبي عروقي‌ـ ريوي‌ـ كليوي‌ـ كبدي‌ـ غدد‌ـ CNS‌ـ چشم، گوش، حلق و بيني‌ـ مامايي‌ـ اطفال‌ـ سالمندان‌ـ پيوند عضو‌ـ جراحي سرپايي‌ـ بيهوشي در خارج اتاق عمل‌ـ ريكاوري‌ـ اداره درد‌ـ ICU‌ـ تروما‌ـ احياء قلبي ريوي.

ضمن تشکر از تمامی افرادی که در تهیه این مجموعه یاری نموده‌اند، اميد است مطالعه اين كتاب مورد استفاده همكاران قرار گيرد.

مراقبتهای بیمار پس از اعمال جراحی قلب باز و CABG

مراقبتهای بیمار پس از اعمال جراحی قلب باز و CABG

پس از عمل جراحی بیماران، مستقیما" بیماران به بخش مراقبت های ویژه منتقل می شود. در آنجا بیمار از بی هوشی در می آید. و در آنجا به مدت 24 تا 48 ساعت بستری می شود.در این زمان تعداد زیادی کاتتر و لوله به بیمار متصل است . اهداف پرستاری فوری بعد از عمل جراحی شامل: حفظ تهویه ی کافی مناسب، اکسیژناسیون و ثبات همودینامیکی است. تشخیص و تدابیر سریع برای هر گونه تغییر در وضعیت بیمار امری مهم و حیاتی است. بعلت  اثرات عمل و دستکاری قلب، بیماری تحت جراحی قلب بیش از سایر بیماران جراحی شده دارای وضعیتی بی ثبات و متغیر شده . پرستار باید با نوع عمل انجام شده، دستورات بعد از عمل و بررسی پیشرفته و مشکل گشایی و مهارت ای  تکنیکی که در این بخش ها سر و کار دارد، آشنا باشد.

 

 
بیمار بعد از ویزیت بوسیله ی متخصص بی هوشی و بررسی تنفس بیمار بر روی مد SIMV  یا ACV وصل می شود. در بعضی از بیماران، بیمار را بر روی 5 سانتی متر آب PEEP نیز قرار می دهند. پرستار باید از جا گذاری لوله ی هوا اطمینان پیدا کند. و  صدا های تنفسی بیمار را سمع کند.
بعد از عمل، بیمار بای هر چه سریع تر به دشتگاه مانیتورینگ متصل شود تا ریتم قلبی و تعداد ضربان قلب را شناسایی کند. اگر بیمار پیس میکر دارد، نحوه ی کار پیس را ارزیابی کند. سطح پتاسیم خون باید 30 دقیقه بعد از عمل بررسی شود. یک نوار EKG از بیمار گرفته شود.
برای کنترل ثبات همودینامیکی باید CVP بیمار چک شود و اگر نیاز بود از دارو های وازو اکتیو یا اینوتروپیک  استفاده شود.
در مورد  درناژ قفسه ی سینه باید این نکته را توجه داشته باشیم که لوله ی درناژ قفسه ی سینه نباید بیش از اندازه خمیده باشد. باید از بدو ورود و هر یک ساعت یک بار مقدار و کیفیت درناژ را مورد ارزیابی قرار دهیم. هموگلوبین و هماتو  کریت بیمار بیمار باید 30 دقیقه بعد از ورود بیمار به بخش مراقبت های ویژه اندازه گیری شود.
اندازه گیری برون ده ادراری باید هر نیم تا یک ساعت یک بار مورد ارزیابی قرار گیرد. بدلیل رقیق شدن خون بیمار در طی عمل، بیمار حجم ادرارش از 100 تا 200 میلی لیتر افزایش می یابد.  وزن مخصوص ادرار در بیمار کاهش می یابد.باید وجود هر گونه  تیرگی در کیسه ی ادرار را مورد توجه قرار دهیم، زیرا نشانه ی وجود هموگلوبین در ادرار است.

بیمار هنگامی که  به بخش می آید دمای بدن بیمار در حدود 35 تا 36 است، پس پس از عمل باید بیمار را گرم نگهداشت و اندازه گیری شود. از افزایش درجه حرارت بدن به دلیل افزایش متابولیسم و بدن و قلب باید پیشگیری کرد.
بررسی بیمار از لحاظ وضعیت بی هوشی حائز اهمیت است. زیرا بیمار در بدو ورودش به بخش به دلیل اثرات دارو های بی هوشی  فاقد هوشیار است و به تدریج بیدار می شود. در نتیجه باید بیمار را مرتبا" به محیط آگاه کنید  و به قوت قلب دهید.

نوشته شده توسط کاوه جعفری

ارزیابی سطح هوشیاری(GCS)

ارزیابی سطح هوشیاری(GCS)

مقیاس کمایی گلاسکو، ابزاری است برای بررسی پاسخ های بیمار نسبت به محرک ها.
نمرات دامنه ای از اعداد 3(کمای عمیق) تا 15(طبیعی) را در بر می گیرند. در این مقیاس 3 معیار اصلی وجود دارد، که عبارتند از: واکش باز کردن چشم ها، بهترین پاسخ کلامی، و بهترین پاسخ حرکتی به فرامین کلامی و محرک های دردناک.این مقیاس به ویژه برای پایش تغییرات ایجاد شده بعد از آسیب دیدگی های سر و غیره مفید واقع شود، اما نمی تواند جایگزین بررسی جامع و کامل وضعیت عصبی شود.
درواکنش باز کردن به چشم ها می تواند خود بخودی باشد، که نمره ی 4 می گیرد، اگر نسبت به صدا واکنش نشان داد نمره 3، اگر به درد واکنش نشان داد نمره 2، و در صورت عدم واکنش نمره1.
اگر از روی آگاهی، بهترین پاسخ کلامی را داد نمره ی 5، در حالت گیجی نمره ی 4، در صورت استفاده  از لغات نا مناسب، نمره ی 3، صوت های غیر قابل درک نمره ی 2، و به عدم پاسخ نمره ی 1 را می دهیم.
بهترین پاسخ حرکتی: اگر بیمار از دستور اطاعت کرد نمره ی 6، اگر با یک تحریک (درد زا) محل درد را تعیین کرد نمره ی 5، اگر خودش را عقب کشید نمره ی 4، اگر خودش را خم کرد نمره ی 3، و اگر باز کرد نمره ی 2، و اگر نسبت به محرک های درد ناک پاسخی نشان نداد نمره ی 1 را می گیرد.
اگر مجموع نمرات، زیر 7 باشد فرد به کما رفته است. و هر چقدر نمره کمتر باشد، کما عمیق تر است.

در فرم تعیین امتیاز اندازه گیری مردمک ها، تعیین ضربان قلب، تعیین فشار خون، تقارن چشم ها باهم، درجه حرارت و ... هست که باید به آنها هم توجه داشت.

 

 

باید توجه داده شود که هر چه میزان GCS پایین تر بیاید، نیاز به عمل جراحی افزایش می یابد.

این مقیاس برای کودکان زیر ۳۶ ماه استفاده نمی شود و از مقیاس PGCS استفاده می شود. در این مقیاس در قسمت کلامی دارای تفاوت تشخیصی برای نمره دهی است. و این تفاوت بخاطر عدم توانایی کودک زیر ۳۶ ماه و عدم تسلط وی در صحبت کردن است و بیشتر تمرکز در این ناحیه بر روی خندیدن و گریه کردن نوزاد و نیز توجه به تحریکات محیطی است.

 

منبع: پرستاری داخلی جراحی برونر- سودارث 2010ترجمه ی زهرا مشتاق انتشارات جامعه نگر 1389

 نوشته شده توسط کاوه جعفری 

 

SEVERE ACUTE RESPIRATORY SYNDROME AND INFLUENZA

SEVERE ACUTE RESPIRATORY SYNDROME AND INFLUENZA

“There is no question that there will be another influenza pandemic someday. We simply don't know when it will occur or whether it will be caused by the H5N1 avian influenza virus. It would be prudent to develop robust plans for dealing with such a pandemic.”^[72]

Influenza A– and severe acute respiratory syndrome (SARS)–associated viruses are examples of respiratory viruses that may have rampant courses, high virulence, and high lethality. SARS struck like a bolt from the blue in 2002 to 2003 and was a grim reminder of our vulnerability to new infectious diseases. SARS affected mainly people in Asia, in the Pacific Rim, and in Canada. The causative agent is thought to be an RNA coronavirus that is passed on through contact and droplet spread. The virus is viable ex vivo for 24 to 48 hours. Many of the victims of the SARS outbreak were health workers, including anesthesiologists. The influenza pandemic of 1918 to 1919 was one of the major plagues to have affected humankind; it is estimated that Spanish flu left a trail of as many as 25 million corpses around the world in just 25 weeks. A new strain of avian influenza, the H5N1 strain, which is a subtype of influenza A, is now threatening humankind. Influenza is an RNA orthomyxovirus, which, like other RNA viruses, mutates at an alarming rate. The strain H5N1 is so named based on the capsular peptides, hemagglutinin, and neuraminidase. There are 16 known hemagglutinin subtypes and nine known neuraminidase subtypes of influenza A viruses. The Spanish flu was caused by an H1N1 strain of the virus, which continues to cause seasonal human influenza. According to the World Health Organization, pathogenic strains of H5N1 that infect humans may be fatal in approximately 66% of cases. Currently, H5N1 influenza A is passed from bird to human. The fear is that if there is recombination within a patient with concurrent H1N1 or H3N2 influenza A infection, the viruses may undergo recombination resulting in a lethal strain that can spread among humans ( Fig. 19-5 ). Patients with acute respiratory viral infections may require care by anesthesiologists for such procedures as emergency intubation, tracheostomy, chest tube placement, mechanical ventilator support, or general ICU care.

 

Management of Anesthesia

Preoperative

The anesthesiologist should assess the patient with an appreciation of the potential lethality of the infection. Both patient and their family should be counseled about the high risks associated with SARS-CoV. These viruses are highly contagious and frequently lethal; strict isolation should be enforced and precautions to protect health workers must be taken. The same may apply to a potential (recombinant or newly evolved) influenza strain. Ideally, infected patients should be cared for in rooms with negative pressure to decrease aerosolized spread and contagion. Barrier precautions include the use of full-body disposable oversuits, double gloves, goggles, and powered air-purifying respirators with high-efficiency particulate air filters. ^{[78] [79]} If these are not available, N95 masks (block 95% of particles) should be used rather than regular surgical masks. Filters should be placed in both limbs of breathing circuits to protect ventilators and anesthesia machines from contamination. All surfaces should be sterilized with alcohol and rooms should ideally not be used for other patients (if practical) for up to 48 hours after a person with SARS-CoV or H5N1 influenza A has been in the room. Even if it is not SARS or influenza, the same principles of infection control barrier precautions apply to any deadly contagious infection, whether occurring “naturally” or introduced by those with malevolent intent.

Intraoperative

Fears about contagion should not blind anesthesiologists to the high level of care required for these vulnerable patients. During the SARS outbreak in Hong Kong, fears about contagion may have affected patient management.^[80] Experience from Canada has shown that when appropriate precautions are taken, spread of infection may be prevented. If mechanical ventilation is required, protective ventilation as for acute respiratory distress syndrome is indicated. Tidal volumes should be limited to 6 to 8 mL/kg lean body mass and mean airway pressure should be less than 30 cm H₂O. Sudden cardiorespiratory compromise could be reflective of an expanding pneumothorax. Draining of pleural effusions may improve ventilation and gas exchange. Care should be taken with bronchoscopy as this is a particularly high-risk procedure that results in aerosolization of viral particles.

Signs and Symptoms

Symptoms include nonspecific complaints of viral infection such as cough, sore throat, headache, diarrhea, arthralgia, and muscle pain. In more severe cases, patients may present with respiratory distress, confusion (encephalitis), and hemoptysis. Signs may include fever, tachycardia, sweating, conjunctivitis, rash, tachypnea, use of accessory respiratory muscles, cyanosis, and pulmonary features of pneumonia, pleural effusions, or pneumothorax. A chest radiograph may show patchy infiltrates, areas of opacification, pneumothoraces, and evidence of pleural effusions. Both H5N1 influenza A virus and SARS-coronavirus (CoV) may cause acute lung injury and acute respiratory distress syndrome. Complications include multiorgan failure and severe sepsis

 

RENAL TRANSPLANTATION

RENAL TRANSPLANTATION

Candidates for renal transplantation are selected from patients with ESRD who are on established programs of long-term hemodialysis. In adults, the most common causes of end-stage renal failure are diabetes mellitus, glomerulonephritis, polycystic kidney disease, and systemic hypertension. Despite concerns about the recurrence of disease in the donor kidney, it has generally been only slowly progressive. A kidney from a cadaver donor can be preserved by perfusion at low temperatures for up to 48 hours, making its transplantation a semielective surgical procedure. Attempts are made to match HLA and ABO blood groups between donor and recipient. Paradoxically, the presence of certain common shared HLA in blood administered to a potential transplant recipient has been observed to induce tolerance to donor antigens and thus improve graft survival. The donor kidney is placed in the lower abdomen and receives its vascular supply from the iliac vessels. The ureter is anastomosed directly to the bladder. Immunosuppressive therapy is instituted during the perioperative period.

Management of Anesthesia

General Anesthesia

Although both regional and general anesthesia have been successfully used for renal transplantation, general anesthesia is most often selected. General anesthesia provides the advantage of mechanically maintaining the patient's ventilation, which may become compromised by surgical retraction in the area of the diaphragm. Drug selection is influenced by known side effects of anesthetic drugs (bowel distention from nitrous oxide, metabolism of sevoflurane to inorganic fluoride). Renal function after kidney transplantation is not predictably influenced by the volatile anesthetic administered. A common approach is to combine volatile anesthetics (isoflurane or desflurane) with nitrous oxide or short-acting opioids. Decreased cardiac output due to negative inotropic effects of volatile anesthetics is minimized to avoid jeopardizing the adequacy of tissue oxygen delivery (especially if anemia is present) and to promote renal perfusion. A high normal systemic blood pressure is required in the presence of euvolemia to maintain adequate urine flow. The selection of muscle relaxants is influenced by the dependence of many of these drugs on renal clearance. In this regard, atracurium, cisatracurium, and mivacurium are attractive selections, as their clearance from the plasma is independent of renal function. A newly transplanted but functioning kidney is able to clear neuromuscular-blocking drugs and the anticholinesterase drugs used for their reversal at the same rate as normal patients.

Central venous pressure monitoring is useful for guiding the rate and volume of crystalloid infusions. Optimal hydration during the intraoperative period is intended to optimize renal blood flow and improve early function of the transplanted kidney. Diuretics are often administered to facilitate urine formation by the newly transplanted kidney. In this regard, osmotic diuretics such as mannitol facilitate urine output and decrease excess tissue and intravascular fluid. Unlike the loop diuretic furosemide, mannitol does not depend on renal tubular concentrating mechanisms to produce diuresis.

When the vascular clamps are released, renal preservative solution from the transplanted kidney and venous drainage from the legs are also released into the circulation. These effluents contain potassium and acid metabolites but, in adults, seem to have minimal systemic effects. Nevertheless, cardiac arrest has been described after completion of the arterial anastomosis to the transplanted kidney and release of the vascular clamp. This event is most likely due to sudden hyperkalemia caused by washout of the potassium-containing preservative solutions from the newly perfused kidney. Unclamping may also be followed by hypotension due to the abrupt addition of up to 300 mL to the capacity of the intravascular fluid space and the release of vasodilating chemicals from previously ischemic tissues. When hypotension results from this change, the treatment is most often intravenous infusion of fluids.

Regional Anesthesia

The advantages of regional anesthesia compared with general anesthesia are the absence of a need for tracheal intubation or administration of neuromuscular blocking drugs. These advantages are negated, however, if regional anesthesia must be extensively supplemented with injected or inhaled drugs. Furthermore, blockade of the peripheral sympathetic nervous system, as produced by regional anesthesia, can complicate control of systemic blood pressure, especially considering the unpredictable intravascular fluid volume status of many of these patients. The use of regional anesthesia, particularly epidural anesthesia, is controversial in the presence of abnormal coagulation.

Postoperative Complications

The newly transplanted kidney may suffer acute immunologic rejection, which manifests in the vasculature of the transplanted kidney. It can be so rapid that inadequate circulation is evident almost immediately after the blood supply to the kidney is established. The only treatment for this acute rejection reaction is removal of the transplanted kidney, especially if the rejection process is accompanied by disseminated intravascular coagulation. A hematoma also may arise in the graft postoperatively, causing vascular or ureteral obstruction.

Delayed signs of graft rejection include fever, local tenderness, and deterioration of urine output. Treatment with high doses of corticosteroids and antilymphocyte globulin may be helpful. The acute tubular necrosis that occurs in the transplanted kidney secondary to prolonged ischemia usually responds to hemodialysis. Cyclosporine toxicity may also cause ARF. Ultrasonography and needle biopsy are performed to differentiate between the possible causes of kidney malfunction.

Opportunistic infections owing to long-term immunosuppression are common after renal transplantation. Long-term survival is unsatisfactory in renal transplant recipients who are immunosuppressed and who also carry hepatitis B surface antigen. The frequency of cancer is 30 to 100 times higher in transplant recipients than in the general population, presumably reflecting the loss of protective effects due to immunosuppression. Large-cell lymphoma is a well-recognized complication of transplantation, occurring almost exclusively in patients with evidence of Epstein-Barr virus infections.

 

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

PNEUMONIA

PNEUMONIA

Combined with influenza, community-acquired pneumonia is one of the 10 leading causes of death in the United States. S. pneumoniae is by far the most frequent cause of bacterial pneumonia in adults. Other bacteria that cause pneumonia include H. influenzae, Mycoplasma pneumoniae, S. aureus, Legionella pneumophilia, K. pneumoniae, and Chlamydia pneumoniae. S. pneumoniae usually causes typical pneumonia. Influenzavirus, M. pneumoniae, chlamydia, legionella, adenovirus, and other microorganisms may cause atypical pneumonia.^[62]

Diagnosis

An initial chill, followed by abrupt onset of fever, chest pain, dyspnea, fatigue, rigors, cough, and copious sputum production often characterize bacterial pneumonia, although symptoms vary. Nonproductive cough is a feature of atypical pneumonias. A detailed history may suggest possible causative organisms. Hotels and whirlpools are associated with Legionnaires' disease (L. pneumoniae) outbreaks. Fungal pneumonia may occur with cave exploration (Histoplasma capsulatum) and diving (Scedosporium angiospermum). Chlamydia psittaci pneumonia may follow contact with birds and Q fever (Coxiella burnetti) contact with sheep. Alcoholism may increase the risk of bacterial aspiration such as K. pneumoniae. Patients who are immunocompromised, such as those with AIDS, are at risk of fungal pneumonia, such as Pneumocystis jiroveci pneumonia (PCP).

Posteroanterior and lateral chest radiographs may be extremely helpful in diagnosing pneumonia.^[63] Diffuse infiltrates are suggestive of an atypical pneumonia whereas a lobar radiographic opacification is suggestive of a typical pneumonia. Atypical pneumonia occurs more frequently in young adults. Radiography is useful for detecting pleural effusions and multilobar involvement. Polymorphonuclear leukocytosis is typical, and arterial hypoxemia may occur in severe cases of bacterial pneumonia. Arterial hypoxemia reflects intrapulmonary shunting of blood owing to perfusion of alveoli filled with inflammatory exudates.

Microscopic examination of sputum plus cultures and sensitivity testing may be helpful in suggesting the etiologic diagnosis of pneumonia and in guiding the selection of appropriate antibiotic treatment. S. pneumoniae and gram-negative organisms, such as H. influenzae, may be seen on sputum stain or culture. Unfortunately, sputum specimens are frequently inadequate and organisms do not invariably grow from sputum. Interpretation of sputum culture may be challenging, as there is frequent normal nasopharyngeal carriage of S. pneumoniae. If there is suspicion, sputum specimens should be sent for acid-fast bacilli (tuberculosis). Antigen detection in urine is a good test for L. pneumophilia. Blood antibody titers are helpful in diagnosing M. pneumoniae. Sputum polymerase chain reaction is useful for chlamydia.^[62] Blood cultures are usually negative, but are important to rule our bacteremia. HIV is an important risk factor for pneumonia and should be tested for when pneumonia is suspected.

Management of Anesthesia

Anesthesia and surgery should ideally be deferred with acute infections. Patients with acute pneumonia are often dehydrated and may have renal insufficiency. However, overly aggressive volume resuscitation may worsen gas exchange and morbidity. Fluid management is therefore extremely challenging. Regional anesthesia may be superior. If general anesthesia is unavoidable, a protective ventilation strategy is appropriate with tidal volumes of 6 to 8 mL/kg ideal body mass and mean airway pressures less than 30 cm H₂O. The anesthesiologist should suction secretions, send distal sputum specimens for Gram stain and culture, and ensure that appropriate antibiotics are administered both for the pneumonia and to cover the surgery.

Postoperative Pneumonia

Postoperative pneumonia occurs in approximately 20% of patients undergoing major thoracic, esophageal, or major upper abdominal surgery but is rare in other procedures in previously fit patients. Chronic respiratory disease increases the incidence of postoperative pneumonia threefold. Other risk factors include obesity, age older than 70 years, and operations lasting more than 2 hours.^[67]

Lung Abscess

Lung abscess may develop after bacterial pneumonia. Alcohol abuse and poor dental hygiene are important risk factors. Septic pulmonary embolization, which is most common in intravenous drug abusers, may also result in formation of a lung abscess. A finding of an air-fluid level on the chest radiograph signifies rupture of the abscess into the bronchial tree, and foul-smelling sputum is characteristic. Antibiotics are the mainstay of treatment of a lung abscess. Surgery is indicated only when complications such as empyema occur. Thoracentesis is necessary to establish the diagnosis of empyema, and treatment requires chest tube drainage and antibiotics. Surgical drainage is necessary to treat chronic empyema.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

MANAGEMENT OF HEART FAILURE

MANAGEMENT OF HEART FAILURE

Current therapeutic strategies are aimed at reversing the pathophysiologic alterations present in heart failure and at interrupting the vicious circle of maladaptive mechanisms ( Fig. 6-3 ). Short-term therapeutic goals in patients with heart failure include relieving symptoms of circulatory congestion, increasing tissue perfusion, and improving the quality of life. However, management of heart failure involves more than the treatment of symptoms. The processes that contributed to the LV dysfunction may progress independently of the development of symptoms. Therefore, the long-term therapeutic goal is to prolong life by slowing or reversing the progression of ventricular remodeling.

Figure 6-3  Primary targets of treatment in heart failure. Treatment options for patients with heart failure affect the pathophysiologic mechanisms that are stimulated in heart failure. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers decrease afterload by interfering with the renin-angiotensin-aldosterone system, resulting in peripheral vasodilation. They also affect left ventricular hypertrophy, remodeling, and renal blood flow. Aldosterone production by the adrenal glands is increased in heart failure. It stimulates renal sodium retention and potassium excretion and promotes ventricular and vascular hypertrophy. Aldosterone antagonists counteract the many effects of aldosterone. Diuretics decrease preload by stimulating natriuresis in the kidneys. Digoxin affects the Na^+K^+ATPase pump in the myocardial cell, increasing contractility. Inotropes such as dobutamine and milrinone increase myocardial contractility. β-Blockers inhibit the sympathetic nervous system and adrenergic receptors. They slow the heart rate, decrease blood pressure, and have a direct beneficial effect on the myocardium by enhancing reverse remodeling. Selected agents that also block α-adrenergic receptors can cause vasodilation. Vasodilator therapy such as combination therapy with hydralazine and isosorbide dinitrate decreases afterload by counteracting peripheral vasoconstriction. Cardiac resynchronization therapy with biventricular pacing improves left ventricular function and favors reverse remodeling. Nesiritide (brain natriuretic peptide) decreases preload by stimulating diuresis and decreases afterload by vasodilation. Exercise improves peripheral blood flow by eventually counteracting peripheral vasoconstriction. It also improves skeletal-muscle physiology.  (Reproduced with permission from Jessup M, Brozena S: Heart failure. N Engl J Med 2003;348:2007–2018. Copyright © 2003 Massachusetts Medical Society. All rights reserved.)

Management of Chronic Heart Failure

The current recommended therapy of chronic heart failure is based on results of large, adequately powered, randomized trials and on the American College of Cardiology/American Heart Association and European Society of Cardiology guidelines for the diagnosis and treatment of chronic heart failure. According to these guidelines, treatment options include lifestyle modification, patient and family education, medical therapy, corrective surgery, implantable devices, and cardiac transplantation ( Fig. 6-4 ).

Figure 6-4  Stages of heart failure and treatment options for systolic heart failure. Patients with stage A heart failure are at high risk of heart failure but do not yet have structural heart disease or symptoms of heart failure. This group includes patients with hypertension, diabetes, coronary artery disease, previous exposure to cardiotoxic drugs, or a family history of cardiomyopathy. Patients with stage B heart failure have structural heart disease but no symptoms of heart failure. This group includes patients with left ventricular hypertrophy, previous myocardial infarction, left ventricular systolic dysfunction, or valvular heart disease, all of whom would be considered to have New York Heart Association (NYHA) class I symptoms. Patients with stage C heart failure have known structural heart disease and current or previous symptoms of heart failure. Their current symptoms may be classified as NYHA class I, II, III, or IV. Patients with stage D heart failure have refractory symptoms of heart failure at rest despite maximal medical therapy, are hospitalized, and require specialized interventions or hospice care. All such patients would be considered to have NYHA class IV symptoms. ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; VAD, ventricular assist device.  (Reproduced with permission from Jessup M, Brozena S: Heart failure. N Engl J Med 2003;348:2007–2018. Copyright © 2003 Massachusetts Medical Society. All rights reserved.)

Lifestyle modifications are aimed at decreasing the risk of heart disease and include smoking cessation, a healthy diet with moderate sodium restriction, weight control, exercise, moderate alcohol consumption, and adequate glycemic control.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

 

Management of Acute Heart Failure

Management of Acute Heart Failure

Patients may experience acute heart failure as a result of decompensated chronic heart failure or de novo. Anesthesiologists deal with acute heart failure when caring for patients in overt heart failure who present for emergency surgery or patients who decompensate intraoperatively. Acute heart failure therapy has three phases: the emergency phase, the in-hospital management phase, and the predischarge phase. For the anesthesiologist, the emergency phase is of most interest and is the phase that is addressed here. The hemodynamic profile of acute heart failure is characterized by high ventricular filling pressures, low cardiac output, and hyper- or hypotension. Traditional therapy includes diuretics, vasodilators, inotropic drugs, mechanical assisted devices (intra-aortic balloon pump, ventricular assist device), and emergency cardiac surgery. Newer therapy includes calcium sensitizers, exogenous BNP, and nitric oxide synthase inhibitors.

Diuretics and Vasodilators

Loop diuretics can improve symptoms rapidly, but in high doses, they may have deleterious effects on clinical outcomes. It may be more desirable to use a combination of a low dose of loop diuretic with an intravenous vasodilator. Nitroglycerin and nitroprusside reduce LV filling pressure and systemic vascular resistance and increase stroke volume. However, nitroprusside may have a negative impact on clinical outcome in patients with acute myocardial infarction.

Inotropic Support

Positive inotropic drugs have been the mainstay of treatment for patients in cardiogenic shock. Their positive inotropic effect is produced via an increase in cyclic adenosine monophosphate, which promotes an increase in intracellular calcium levels and, thereby, an improvement in excitation-contraction coupling. Catecholamines (epinephrine, norepinephrine, dopamine, and dobutamine) do so by direct β-receptor stimulation, whereas phosphodiesterase inhibitors (amrinone, milrinone) block the degradation of cyclic adenosine monophosphate. Side effects of inotropic drugs include tachycardia, increased myocardial energy demand and oxygen consumption, dysrhythmias, worsening of DHF, and down-regulation of β-receptors. Long-term use of these drugs may result in cardiotoxicity and accelerate myocardial cell death.

Calcium Sensitizers

Myofilament calcium sensitizers are a new class of positive inotropic drugs that increase contractility without increasing intracellular levels of calcium. Therefore, there is no significant increase in myocardial oxygen consumption or heart rate and no propensity for dysrhythmias. The most widely used medication in this class is levosemindan. It is an inodilator increasing myocardial contractile strength and promoting dilation of systemic, pulmonary, and coronary arteries. It does not worsen diastolic function. Studies have shown that levosemindan may be particularly useful in the setting of myocardial ischemia. Levosemindan is included in the European guidelines for treatment of acute heart failure, but it is not yet available for use in the United States.

Exogenous B-Type Natriuretic Peptide

Nesiritide (Natrecor) is recombinant BNP that binds to both the A- and B-type natriuretic receptors. It promotes arterial, venous, and coronary vasodilation, thereby decreasing LVEDP and improving dyspnea. Nesiritide induces diuresis and natriuresis. It has many effects similar to nitroglycerin but generally produces less hypotension and more diuresis than nitroglycerin.

Nitric Oxide Synthase Inhibitors

The inflammatory cascade stimulated by heart failure results in production of a large amount of nitric oxide in the heart and vascular endothelium. These high levels of nitric oxide have a negative inotropic and profound vasodilatory effect leading to cardiogenic shock and vascular collapse. Inhibition of nitric oxide synthase should decrease these harmful effects. L-NAME (N-nitro-L-arginine methyl ester) is the principal drug in this class under investigation.

Mechanical Devices

If the etiology of acute heart failure is a large myocardial infarction, the insertion of an intra-aortic balloon pump should be considered. The intra-aortic balloon pump is a mechanical device inserted via the femoral artery and positioned just below the left subclavian artery. Its balloon inflates in diastole increasing aortic diastolic blood pressure and coronary perfusion pressure. The balloon deflates in systole creating a “suction” effect that enhances LV ejection. Complications of intra-aortic balloon pump placement include femoral artery or aortic dissection, bleeding, thrombosis, and infection.

In severe cardiogenic shock, emergency insertion of LV and/or right ventricular assist devices may be necessary for survival.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

 

EPIDERMOLYSIS BULLOSA

EPIDERMOLYSIS BULLOSA

Epidermolysis bullosa is a group of genetic diseases of mucous membranes and skin, particularly the oropharynx and esophagus. Epidermis bullosa can be categorized as simplex, junctional, and dystrophic. In the simplex type, epidermal cells are fragile and mutations of genes encoding keratin intermediate filament proteins underlie the fragility. In the dystrophic types (incidence approximately one in every 300,000 births), the genetic mutation appears to be in the gene encoding the type of collagen that is the major component of anchoring fibrils

Management of Anesthesia

Supplemental corticosteroids may be indicated during the perioperative period if patients have been on long-term treatment with these drugs. The main anesthetic concerns in patients with epidermolysis bullosa center on the serious complications that can occur if proper precautions are not taken during instrumentation. Avoidance of trauma to the skin and mucous membranes is crucial. Bulla formation can be caused by trauma from tape, blood pressure cuffs, tourniquets, adhesive electrodes, and rubbing the skin with alcohol wipes. Blood pressure cuffs should be padded with a loose cotton dressing. Electrodes should have the adhesive portion removed. Petroleum jelly gauze can help hold them in place. Anything that touches a patient should be well padded. Intravenous and intra-arterial catheters should be sutured or held in place with gauze wraps rather than tape. A nonadhesive pulse oximetry sensor should be used. A soft foam, sheepskin, or gel pad should be placed under the patient. All creases should be removed from the linen.

Trauma from the anesthetic face mask must be minimized by gentle application against the face. Lubrication of the face and mask with cortisol ointment, or indeed any lubricant, can be helpful. Upper airway instrumentation should be minimized because the squamous epithelium lining the oropharynx and esophagus is very susceptible to trauma. Frictional trauma to the oropharynx, such as that produced by an oral airway, can result in formation of large intraoral bullae and/or extensive hemorrhage from denuded mucosa. Nasal airways are equally hazardous. Esophageal stethoscopes should be avoided. Hemorrhage from ruptured oral bullae has been treated successfully with epinephrine-soaked gauze applied directly to the bullae.

Interestingly, endotracheal intubation has not been associated with laryngeal or tracheal complications in patients with epidermolysis bullosa dystrophica. Indeed, laryngeal involvement with this form of the disease is rare, and tracheal bullae have not been reported. This finding is consistent with the greater resistance of columnar epithelium to disruption compared to fragile squamous epithelium. Generous lubrication of the laryngoscope blade with cortisol ointment and/or petroleum jelly and selection of a smaller endotracheal tube than usual are recommended. Chronic scarring of the oral cavity can result in a narrow oral aperture and immobility of the tongue making tracheal intubation difficult. After intubation, the tube must be carefully immobilized with soft cloth bandages to prevent movement in the oropharynx, and the tube must be positioned so that it does not exert lateral forces at the corners of the mouth. Tape is not used to hold the endotracheal tube in place. It must be remembered that oropharyngeal suctioning can lead to life-threatening bulla formation. The risk of pulmonary aspiration may be increased in the presence of esophageal stricture.

Porphyria cutanea tarda has been reported to occur with increased frequency in patients with epidermolysis bullosa. This type of porphyria does not have the same implications for management of anesthesia, as does acute intermittent porphyria.

Propofol and ketamine are useful for avoiding airway manipulation when the operative procedure does not require controlled ventilation or skeletal muscle relaxation. Despite the presence of dystrophic skeletal muscle, there is no evidence that these patients are at increased risk of a hyperkalemic response when treated with succinylcholine. There are no known contraindications to the use of volatile anesthetics in these patients. As alternatives to general anesthesia, regional anesthetic techniques (spinal, epidural, brachial plexus block) have been recommended.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

 

Colorectal Cancer

Colorectal Cancer

Colon cancer is second only to lung cancer as a cause of cancer death in the United States. The incidence and mortality from this cancer has not changed appreciably during the past several decades. Almost all colorectal cancers are adenocarcinomas, and the disease generally occurs in adults older than 50 years.

Etiology

Most colorectal cancers arise from premalignant adenomatous polyps. Large polyps, especially those larger than 1.5 cm in diameter, are more likely to contain invasive cancer. Although adenomatous polyps are common (present in more than 30% of patients older than 50 years), less than 1% of adenomatous polyps ever become malignant. It is thought that adenomatous polyps require at least 5 years of growth before they become clinically significant. The evolution of normal colonic mucosa to a benign adenomatous polyp that contains cancer and then to life-threatening invasive cancer is associated with a series of genetic events that involve the mutational activation of a proto-oncogene and the loss of several genes that normally suppress tumorigenesis.

Most colorectal cancers appear to be related to diet, with the disease occurring in the greatest incidence among individuals in upper socioeconomic classes living in urban areas. There is a direct correlation between calories consumed, dietary fat and oil, and meat protein. Available data indicate that a high intake of animal fat is the dietary element that is most strongly associated with the risk of colon cancer. As many as 25% of patients with colorectal cancer have a family history of the disease. Inflammatory bowel disease is associated with an increased incidence of colorectal cancer. Cigarette smoking for longer than 35 years appears to increase the risk of colorectal cancer.

Diagnosis

The rationale for colorectal cancer screening is that early detection and removal of localized superficial tumors and precancerous lesions in asymptomatic individuals increases the cure rate. Screening programs (digital rectal examination, examination of the stool for occult blood, colonoscopy) appear to be particularly useful for persons who have first-degree relatives with a history of the disease, especially if these relatives developed the colorectal cancer before 55 years of age. There is evidence that annual or biennial fecal occult blood testing is associated with a decreased incidence of colorectal cancer.

Signs and Symptoms

The presenting signs and symptoms of colorectal cancer reflect the anatomic location of the cancer. Because stool is relatively liquid as it passes into the right colon through the ileocecal valve, tumors in the cecum and ascending colon can become large and markedly narrow the bowel lumen without causing obstructive symptoms. Ascending colon cancers frequently ulcerate, leading to chronic blood loss in the stool. These patients experience symptoms related to anemia, including fatigue and, in some patients, angina pectoris.

Stool becomes more concentrated as it passes into the transverse colon. Transverse colon cancers cause abdominal cramping, occasional bowel obstruction, and even perforation. Abdominal radiographs reveals characteristic abnormalities in the colonic gas pattern, reflecting narrowing of the lumen (“napkin ring lesion”). Colon cancers developing in the rectosigmoid portion of the large intestine result in tenesmus and thinner stools. Anemia is unusual despite the passage of bright red blood from the rectum (often attributable to hemorrhoids).

Colorectal cancers initially spread to regional lymph nodes and then through the portal venous circulation to the liver, which represents the most common visceral site of metastases. Colorectal cancers rarely spread to lung, bone, or brain in the absence of liver metastases. A preoperative increase in the serum concentration of carcinoembryonic antigen suggests that the tumor will recur following surgical resection. Carcinoembryonic antigen is a glycoprotein that is also increased in the presence of other cancers (stomach, pancreas, breast, lung) and nonmalignant conditions (alcoholic liver disease, inflammatory bowel disease, cigarette smoking, pancreatitis).

Treatment

The prognosis for patients with adenocarcinoma of the colorectum depends on the depth of tumor penetration into the bowel wall and the presence or absence of regional lymph node involvement and distant metastases (liver, lung, bone). Radical surgical resection, which includes the blood vessels and lymph nodes draining the involved bowel, offers the best potential for cure. Surgical management of cancers that arise in the distal rectum may necessitate a permanent sigmoid colostomy (abdominoperineal resection). Because most recurrences occur within 3 to 4 years, the cure rate for colorectal cancer is often estimated by 5-year survival rates.

Radiation therapy is a consideration in patients with rectal tumors since the risk of recurrence following surgery is significant. Postoperative radiation therapy causes transient diarrhea and cystitis, but permanent damage to the small intestine and bladder is uncommon. Use of chemotherapy in patients with advanced colorectal cancers rarely results in a satisfactory response.

Management of Anesthesia

Management of anesthesia for surgical resection of colorectal cancers may be influenced by anemia and the effects of metastatic lesions in liver, lung, bone, or brain. Chronic large bowel obstruction probably does not increase the risk of aspiration during induction of anesthesia, although abdominal distention could interfere with adequate ventilation and oxygenation. Blood transfusion during surgical resection of colorectal cancers has been alleged to be associated with a decrease in the length of patient survival. This could reflect immunosuppression produced by transfused blood. For this reason, careful review of the risks and benefits of blood transfusions in these patients is prudent.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

CIRRHOSIS

CIRRHOSIS

Cirrhosis can result from a large variety of chronic, progressive liver diseases. Most often cirrhosis is the result of excessive chronic alcohol ingestion or chronic viral hepatitis due to HBV or HCV infection. Scarring of the liver results in disruption of normal liver architecture, and regenerating parenchymal nodules are typically seen. The pattern of scarring seldom permits determination of a specific etiology, but other histologic features may provide clues as to the cause of the cirrhosis.

Diagnosis

Percutaneous liver biopsy establishes the diagnosis of cirrhosis. Computed tomography, magnetic resonance imaging, and hepatic ultrasonography with Doppler flow studies may reveal findings consistent with cirrhosis (splenomegaly, ascites, irregular liver surface). Upper gastrointestinal endoscopy can establish the presence of esophagogastric varices.

Management of Anesthesia

It is estimated that 5% to 10% of patients with cirrhosis require surgery in the last 2 years of life. Many trauma beds are occupied by patients who were injured while under the influence of alcohol. In those patients who abuse alcohol, the presence of ascites, sepsis, and chronic obstructive pulmonary disease preoperatively is associated with increased postoperative morbidity and mortality. Postoperative morbidity includes pneumonia, bleeding, sepsis, poor wound healing, and deterioration in liver function. The pathogenic mechanisms of these complications often includes subclinical cardiorespiratory insufficiency and immune incompetence. The complications of alcohol withdrawal can also affect perioperative morbidity.

Preoperative Preparation

Certain preoperative criteria correlate with surgical risk and postoperative outcome in patients with cirrhosis undergoing major surgery ( Table 11-6 ). Identifying co-existing problems that can be optimized preoperatively (cardiorespiratory function, coagulation status, renal function, intravascular fluid volume, electrolyte balance, nutrition) may decrease morbidity and mortality associated with elective surgery in patients with severe liver disease. Coagulation status should be evaluated and parenteral vitamin K administered if the prothrombin time is prolonged. Failure of parenteral vitamin K to improve synthesis of prothrombin suggests the presence of severe hepatocellular disease. Impaired prothrombin production due to biliary obstruction and the absence of bile salts that facilitate gastrointestinal absorption of vitamin K is promptly reversed by parenteral vitamin K therapy. Thrombocytopenia, which often accompanies severe liver disease, may require treatment. Hypoglycemia may be present, and administration of a glucose solution is a consideration perioperatively. There should be proper hydration and urine output prior to surgery. Hepatic blood flow is predictably decreased in patients with cirrhosis, and any further decrease due to anesthetic-induced depression of cardiac output or blood pressure could jeopardize hepatocyte oxygenation.

TABLE 11–6   -- Prediction of Perioperative Risk in the Patient with Liver Disease

Parameter	Low Risk	Moderate Risk	High Risk
Bilirubin (mg/dL)	<2	2–3	>3
Albumin (g/dL)	>3.5	3.0–3.5	<3
Prothrombin time (seconds prolonged)	1–4	4–6	>6
Encephalopathy	None	Moderate	Severe
Nutrition	Excellent	Good	Poor
Ascites	None	Moderate	Marked

Adapted from Strunin I: Preoperative assessment of the patient with liver dysfunction. Br J Anaesth 1978;50:25–34.

 

Chronic alcohol ingestion has been demonstrated to increase anesthetic requirements (MAC) for isoflurane most likely due to cross-tolerance. Accelerated metabolism of drugs in the presence of alcohol-induced microsomal enzyme induction can also alter the amount of anesthetic drug needed to achieve a certain anesthesia depth. Decreased protein binding of drugs in the presence of hypoalbuminemia could increase the pharmacologically active fraction of intravenous anesthetic drugs. Alcohol-induced cardiomyopathy could make patients unusually sensitive to the cardiac depressant effects of volatile anesthetics. There may be decreased responsiveness to catecholamines.

Intoxicated Alcoholic Patients

In contrast to a chronic but sober alcoholic patient, the acutely intoxicated patient requires less anesthetic because there are additive depressant effects from the alcohol and the anesthetic drugs. Acutely intoxicated patients are also ill equipped to withstand stress and acute surgical blood loss. Furthermore, alcohol may decrease the tolerance of the brain to hypoxia. Intoxicated patients may be more vulnerable to regurgitation of gastric contents since alcohol delays gastric emptying and decreases lower esophageal sphincter tone. Surgical bleeding may reflect alcohol-induced interference with platelet aggregation. Alcohol, even in moderate doses, causes increased plasma catecholamine concentrations, most likely reflecting inhibition of neurotransmitter uptake back into presynaptic nerve endings.

Intraoperative Management

Optimal anesthetic drug choices or techniques in the presence of liver disease are unknown. It is important to remember, however, that a constant feature of chronic liver disease is decreased hepatic blood flow due to portal hypertension. As a result, hepatic blood flow and hepatocyte oxygenation are more dependent on hepatic artery blood flow than normally. The hepatic artery may provide more than 50% of the oxygen supply by vasodilating during periods of decreased portal vein blood flow. Hepatic blood flow and hepatocyte oxygenation seem to be well maintained during administration of isoflurane, desflurane, and sevoflurane but not halothane. However, the ability of the hepatic artery to vasodilate in response to a decrease in portal vein blood flow can be blunted by volatile anesthetics, especially halothane and especially in high concentrations. It is prudent to limit the dose of volatile anesthetic to minimize the likelihood of a persistent decrease in mean arterial pressure because intraoperative hypotension may be associated with increased postoperative morbidity and mortality. Intravenous anesthetic drugs are valuable adjuncts to volatile anesthetics with or without nitrous oxide, but cumulative drug effects are likely if liver disease is severe enough to slow metabolism of the intravenous anesthetics. Regardless of the drugs selected for anesthesia, postoperative liver dysfunction is likely to be exaggerated in patients with chronic liver disease, presumably due to the effects of anesthetic drugs and/or stress-induced activation of the sympathetic nervous system on hepatocyte oxygenation. Regional anesthesia can be useful in patients with advanced liver disease if the coagulation status is acceptable.

Muscle Relaxants

Hepatic clearance of muscle relaxants must be considered when selecting a particular neuromuscular blocker for administration to patients with cirrhosis. Succinylcholine or mivacurium are acceptable, although severe liver disease may decrease plasma cholinesterase activity and prolong the duration of action of these drugs. The increased volume of distribution that accompanies cirrhosis, especially with ascites, will result in the need for a larger initial dose of nondepolarizing muscle relaxant to produce the required plasma concentration. However, subsequent doses may be smaller due to decreased hepatic clearance and metabolism. Hepatic dysfunction does not alter the elimination half-time of atracurium or cisatracurium. The elimination half-time of vecuronium is not increased until the dose exceeds 0.1 mg/kg, consistent with the dependence of this drug on hepatic clearance. Altered protein binding of muscle relaxants is insignificant as a mechanism of an altered response in patients with cirrhosis.

Monitoring

Monitoring of arterial blood gases and urine output is often necessary. The need for invasive intraoperative monitoring is determined by the extent and urgency of the surgery. Management of anesthesia for surgical creation of a portocaval shunt includes monitoring arterial pressure and cardiac filling pressures. Fluid administration must be carefully titrated to an endpoint such as central venous pressure, pulmonary artery occlusion pressure, and urine output. Intraoperative maintenance of an acceptable urine output may help decrease the risk of postoperative acute renal failure. When blood replacement is necessary, the stored blood should be administered as slowly as possible to compensate for the decreased clearance of citrate by the cirrhotic liver. Infusion of glucose may be necessary during the perioperative period to prevent hypoglycemia. A practical point is avoidance of unnecessary esophageal instrumentation (esophageal stethoscope, orogastric or nasogastric tube) in patients with known esophageal varices.

Postoperative Management

Regardless of the drugs selected for anesthesia, postoperative liver dysfunction/jaundice is likely in patients with chronic liver disease. Cholestasis and sepsis can also be causes of postoperative jaundice. Manifestations of alcohol withdrawal usually appear 24 to 72 hours after cessation of drinking and can constitute a medical emergency in the postoperative period.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

ACUTE LIVER FAILURE

ACUTE LIVER FAILURE

Acute hepatic failure is characterized by jaundice, hypoalbuminemia, coagulopathy, malnutrition, susceptibility to infection, and renal dysfunction in the clinical setting of acute hepatic disease. Fulminant hepatic failure refers to acute liver failure with superimposed hepatic encephalopathy that develops within 2 to 8 weeks of the onset of illness in a patient without preexisting liver disease. Viral hepatitis and drug-induced liver injury account for most cases of acute liver failure

Management of Anesthesia

Only surgery necessary to correct life-threatening problems should be considered in patients with acute liver failure. Preoperative correction of coagulation abnormalities with fresh frozen plasma may be indicated. Low doses of volatile anesthetics or even nitrous oxide alone may be sufficient to provide analgesia and amnesia in these critically ill patients. Intravenous anesthetics may have prolonged effects due to the marked reduction in metabolism of these drugs. Muscle relaxants may be needed to facilitate operative exposure or manage ventilation. When choosing a muscle relaxant, one must consider the impact of decreased hepatic function and associated renal dysfunction on the clearance of the drug. Because the plasma half-life of pseudocholinesterase is 14 days, it is unlikely that acute liver failure would be associated with a prolonged response to succinylcholine or mivacurium.

Administration of glucose is important, and plasma glucose measurement to confirm the absence of hypoglycemia is prudent. Blood should be administered as slowly as possible to minimize the likelihood of citrate intoxication. Monitoring arterial blood gases and electrolyte concentrations is helpful since these patients are vulnerable to development of arterial hypoxemia, metabolic acidosis, hypokalemia, hypocalcemia, and hypomagnesemia. Hypotension and its adverse effect on hepatic blood flow and hepatocyte oxygenation must be considered. Urine output is maintained with intravenous infusion of crystalloid or colloid and, if necessary, diuretic administration. Invasive monitoring is helpful for guiding overall hemodynamic management. These patients are vulnerable to infection, emphasizing the importance of aseptic technique during insertion of intravascular catheters. Lactulose therapy during the preoperative period may decrease the ammonia load and help prevent development of hepatic encephalopathy.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com