By E. Angir. Milligan College. 2018.
Newer preservative agents may tion are reported at 92% cheap 20mg protonix mastercard, 78% cheap protonix 20mg without a prescription, 62% discount 40 mg protonix free shipping, and 50%, increase this time period and permit a larger area respectively, for 1 month, and 1, 3, and 5 years, as for donor allocation. Early mortality Period (ie, at 30 days) is most often to the result of pri- mary graft failure, mortality between 30 days and Patients are typically discharged from the hos- 1 year is most often to the result of infection, and pital within 7 to 14 days after surgery. Some institutions perform surveillance bron- The degree of improvement in lung function choscopy on a routine schedule to detect asymp- postoperatively is the product of many factors. Pathology from exercise testing generally reveals a reduction in biopsy specimens, autopsy specimens, or lung maximum oxygen consumption to 40 to 60% of explants removed during retransplantation reveals predicted in all transplant groups. Reports15,16 have documented the successful use large majority of patients have expressed satisfac- of protective ventilatory strategies, nitric oxide, tion with their transplant decision. The investigators found transplant complications and the approximate time an incidence of 15% for this complication, and it period in which they usually occur. The theoretical causes of airway complications Acute Rejection: Acute rejection can develop include ischemia at the site of the anastomosis, in up to 50% of patients in the ﬁrst postoperative infection, poor organ preservation, and/or rejec- month, and as many as 90% of patients will have at tion. In patients with severe Clinically, patients with acute rejection present rejection, the alveolar space may be involved, and with cough, shortness of breath, malaise, and fever. Mainte- episodes; however, in those episodes of rejection nance immunosuppression therapy should also occurring after 1 month after transplantation only be augmented. Recurrent noted with acute rejection include a perihilar or persistent acute rejection may initiate conver- ﬂare, and alveolar, or interstitial, localized, or dif- sion in the baseline immunosuppression regimen. Methotrexate, total lympholytic radia- mucociliary clearance, recipient-harbored infection tion, aerosolized cyclosporine, photopheresis, and and, occasionally, the transfer of infection from the newer immunosuppressive agents have been used donor organ. Inhaled the surgical wound, vascular access, and urinary corticosteroids may be added to therapy in cases tract or ventilator-associated pneumonias also of lymphocytic bronchiolitis. In most shown beneﬁt from the use of low-dose azithromy- circumstances, the allograft or graft is the primary cin (via an antiinﬂammatory mechanism) for treat- location of infection. The incidence of perioperative bacterial antibiotics or suppressive quinolone treatment may pneumonia has been decreased to as low as 10% by be considered. The prevalence of In addition, the limited donor supply does not bacterial pneumonia remains high during the ﬁrst allow for the common practice of this procedure. It is often difficult to distinguish pneumo- Infections have been a major cause of early nia from other early graft complications such as and late morbidity and mortality after transplan- reperfusion injury, pulmonary edema, rejection, tation, and they remain the leading single speciﬁc and other infectious etiologies. Acyclovir amphotericin B, azoles (particularly itraconazole prophylaxis for herpes infection is initiated in most for 3 to 6 months), or aerosolized amphotericin programs after the discontinuation of therapy with has shown promise in decreasing the incidence of ganciclovir. Fungal infections ac- tive for infections caused by Candida albicans, but count for the most signiﬁcant morbidity and mortal- amphotericin B is still the agent of choice for a ity of all infectious agents after transplantation, and widespread disease. Aspergillus species amphotericin B remains the antifungal agents of exhibits the propensity to invade blood vessels and choice for these infections, although azole agents may present as an infarct or with hemoptysis. Other forms of Posttransplant Lymphoproliferative Disorders presentation of Aspergillus infection can include pseudomembranous tracheobronchitis, often at and Posttransplant lymphoproliferative disorders distal to the site of the anastomosis. Some programs have completely discon- fact that the lymphatics are not reanastomosed tinued the use of prednisone after 1 year after after transplant and/or in the setting of rejection. This complication may be more with complications, which can pose a signiﬁcant common in those patient populations predisposed problem after transplantation (Table 4). Osteoporosis remains a signiﬁcant problem transcription, thus decreasing T-lymphocyte acti- in the posttransplant period and is best managed vation and subsequent proliferation. In addition, other potentially nephrotoxic therapy with azole agents without increasing the agents, including amphotericin B, trimethoprim- dose of cyclosporine or tacrolimus can result in sulfamethoxazole, nonsteroidal antiinﬂammatory an acute and life-threatening drop in therapeutic agents, and aminoglycoside antibiotics, which may levels of these drugs. Interactions with macrolide compound the toxic effects of cyclosporine and antibiotics, calcium-channel blockers, and gastric tacrolimus, may be used in transplant patients. Levels of Both cyclosporine and tacrolimus are also asso- both agents are decreased with the use of rifampin ciated with systemic hypertension, which can or anticonvulsant agents. The incidence of both Toxicities of this drug include cytopenias such as posttransplant hypertension and hyperlipidemia leukopenia and thrombocytopenia. Other well-described side effects of creatitis and cholestatic hepatitis have been well tacrolimus and cyclosporine include neurologic described with azathioprine use. Impact 3 with the cytokine release syndrome manifested by of body weight on long-term survival after lung hypotension, noncardiogenic pulmonary edema, transplantation. Infection the activation of T cells, B cells, and other cell lines with Burkholderia cepacia in cystic ﬁbrosis: outcome by cytokines and growth factors, thus preventing following lung transplantation. The use of sirolimus in vival of lung transplant patients with cystic ﬁbrosis the immediate posttransplant period is discour- harboring panresistant bacteria other than Burk- aged because of the association with bronchial holderia cepacia, compared with patients harboring anastomotic dehiscence when used in combination sensitive bacteria. Impact of a thrombocytopenia and leukopenia), hyperlipid- lung transplantation donor-management protocol emia, arthralgias, and interstitial pneumonitis, on lung donation and recipient outcomes. A survey try of the International Society for Heart and Lung of clinical practice of lung transplantation in North Transplantation: twenty-ﬁfth ofﬁcial adult lung and America. Eur Respir J 2003; 22:1007–1018 and for clinical staging of chronic dysfunction in A review article discussing pathogenesis, risk factors, clinical lung allografts: International Society for Heart and presentation, diagnosis, and treatment of bronchiolitis oblit- Lung Transplantation. It presents data on after onset of bronchiolitis obliterans syndrome in lung indications, numbers, survival, rates of morbidity and mortal- transplant recipients.
However protonix 20 mg free shipping, in hypovolaemia and hypotension resulting in tissue hypoxia best protonix 40mg, anaerobic metabolism in the tissues results in lactic acidosis protonix 20mg low cost. In pre-renal oliguria, the Acute Renal Failure 171 Handbook of Critical Care Medicine concentration ability of the kidney is preserved, while it is lost in intrinsic renal failure. This will depend on the cause, and urgent referral to a genitourinary surgeon is necessary. Acute Renal Failure 172 Handbook of Critical Care Medicine Treatment of pre-renal oliguria Look for features of acute circulatory impairment; tachycardia, hypotension, cold extremities, lactic acidosis, high blood urea – these are present after loss of more than 10-15% of blood volume. Note that a fluid challenge should be tried in oliguric patients even if the patient is normotensive, if other signs of intravascular volume depletion are present. Acute circulatory impairment could be classified as being with either distended neck veins, or flat neck veins. Distended neck veins will be seen in cardiogenic shock; associated hypovolaemia may still be present – however, fluids should be given with care, as the patient could be pushed into pulmonary oedema. It may be necessary to treat heart failure concurrently, with diuretics and inotropes. Note that even in cardiogenic shock, fluids may be required; hypovolaemia will result in reduced preload and (based on the Frank-Starling Law) further reduce cardiac contractility. Colloids – hetastarch is an alternative, however, x There is no proven benefit of colloids over crystalloids, although theoretically colloids stay in the intravascular compartment, and crystalloids are distributed equally in the intravascular and extravascular compartments. Look for haemodynamic improvement – rise in blood pressure, fall in tachycardia, rise in oxygen saturation, rise in jugular venous pressure, and most importantly, improvement in urine output. In the study by Rivers et al on early and aggressive fluid resuscitation in critically ill patients, large volumes (upto several litres) were given effectively and safely. Watch carefully for over hydration and pulmonary oedema, which is the main risk involved in giving fluids; the patient may complain of dyspnoea and become tachypnoeic, and develop fine basal crackles. Should pulmonary oedema Acute Renal Failure 173 Handbook of Critical Care Medicine develop, fluids should be stopped. Pathetically low volumes of fluids are given, and lack of response is interpreted as failure of the fluid challenge test. It is much easier to manage pulmonary oedema than it is to manage the disastrous complications of renal and multi-organ failure resulting from prolonged tissue hypoperfusion caused by inadequate intravascular volume. Ventilated patients are relatively protected from pulmonary oedema due to fluid overload, and hence larger volumes of fluids can be safely given. If the blood pressure does not respond to fluids, cardiogenic or septic shock is likely. In cardiogenic shock, the neck veins are likely to be distended, and pulmonary oedema may be present. In septic shock, the blood pressure may not respond to fluids; this is because of the profound vasodilatation that occurs. Noradrenaline is the most effective in terms of raising blood pressure and improving renal perfusion. Dobutamine worsens vasodilatation, and should only be added to noradrenaline if cardiac dysfunction is present. Replacement doses of corticosteroids may be necessary to restore vascular sensitivity to vasopressors (see section on Severe Sepsis and septic shock). Reno-protection Apart from fluid resuscitation, the following steps should be taken to prevent renal damage x Avoidance of nephrotoxic drugs. Acute Renal Failure 174 Handbook of Critical Care Medicine Management of Renal oliguria The initial evaluation has been dealt with above. Acute Renal Failure 175 Handbook of Critical Care Medicine Treatment Most of the time, acute tubular necrosis has occurred. In addition, patients may be hypovolaemic which contributes to oliguria, and a cautious trial of fluids could be given. The patient with renal oliguria is unable to excrete fluids, and hence can easily develop fluid overload. The main problems in renal failure are: x Uraemia: o Uraemic encephalopathy- anorexia, nausea, vomiting, malaise, confusion, coma. Space is often necessary to give inotropes, antibiotics, blood and blood products. Fluid overload also results in pulmonary congestion, increased risk of lung infections, and difficulties in ventilation, and can make cardiac failure worse. If the patient is euvolaemic, then the aim is to maintain euvolaemia, by replacing urinary and insensible losses. Usually, daily intake should be the previous day’s urine output + around 500-600ml (insensible loss). On average, the required hourly output is – the previous hour’s urine output + 20-25ml. This should be balanced off every 4 hours, as administration of drugs and blood products will result in different obligatory intakes at different times of the day.
Typi- monary edema associated with opiate exposure cally generic protonix 20mg otc, therapy with the implicated drug is with- and suggested that there was a pathophysiologic drawn order 20mg protonix amex, and a trial of corticosteroids is considered buy protonix 20 mg overnight delivery, relationship. In 1972, Edward Rosenow1 exten- particularly in the setting of signiﬁcant symptoms sively reviewed this topic and identiﬁed 20 drugs and/or gas-exchange abnormalities. Major Clinical Syndromes of Drug-Induced implicated in causing a wide array of pulmonary Pulmonary Disease manifestations that involve virtually all com- 1. Patients can Chronic Pneumonitis/Fibrosis present with Loefﬂer syndrome, consisting of an acute onset over several days of cough, dyspnea, A wide array of drugs has been implicated in fever, rash, myalgias, peripheral eosinophilia, and causing chronic interstitial pneumonitis and/or fleeting infiltrates. Alternatively, patients may ﬁbrosis, making them the most common manifes- present with chronic eosinophilic pneumonia tations of drug-induced lung disease. These (eg, restrictive physiology), a reduced diffusing patients generally present with acute dyspnea and capacity of the lung for carbon monoxide (Dlco), a nonproductive cough that develops during a and arterial hypoxemia at rest or with exercise. First, some drugs increase a high clinical suspicion, lung biopsy, prompt the ﬁltration coefﬁcient of the respiratory mem- withdrawal of therapy with the implicated drug, brane, making it more permeable (eg, overdose and the administration of corticosteroids. For example, pulmonary edema associated that induce respiratory depression or block respira- with an overdose of salicylates is potentially tory muscle function. Patients with underlying reversible with appropriate management, whereas pulmonary or neuromuscular disorders are par- patients with carmustine-induced pulmonary ticularly prone to the development of acute hyper- edema generally have a poor prognosis. Some of the agents implicated in causing neuromuscular blockade or Cryptogenic Organizing Pneumonia motor neuropathies/myopathies are listed in Table 6. Gold and clinical suspicion to identify the offending drug penicillamine, the two best-characterized etiologic and withdrawal of therapy with the agent to avoid agents, are often used in the management of further respiratory failure. Cough often occurs in patients with drug- • Captopril • Phenytoin induced bronchospasm or drug-induced interstitial • Corticosteroids • Procainamide lung disease. Chronic pleural an enhanced 5-lipoxygenase pathway, resulting in effusion may occur after long-term exposure to the production of bronchoconstricting cysteinyl- drugs that induce a delayed hypersensitivity-type leukotrienes and, to a lesser extent, by a reduction response (eg, methotrexate or procarbazine) or in in bronchodilating prostaglandins (eg, prostaglan- association with the development of interstitial din E2). Gold and penicillamine cause irre- agents, including some of the newer antineoplastic versible airways obstruction due to concentric agents, are associated with an increased risk of bronchiolitis obliterans. Oral contraceptives and other estrogen-containing agents have also been asso- Drugs that affect the pulmonary vascular cir- ciated with an increased risk of pulmonary culation by causing venous thromboembolism hypertension. A case-control study10 62 cases from 40 publications, 7 of whom were showed that appetite suppressants (eg, amphet- entirely steroid naïve (eg, not receiving any form amines, fenﬂuramine, and dexfenﬂuramine) are of inhaled or oral steroids when symptoms devel- associated with an increased risk of primary pul- oped), suggesting that there may be a causal rela- tionship. Chest Reactions radiograph abnormalities include pleural effu- sions, atelectasis, diffuse interstitial inﬁltrates, and There are a variety of less common drug- alveolar inﬁltrates. Abciximab, a chimeric monoclo- patients receiving doses of 400 mg/d but can be nal antibody directed against platelet glycoprotein found in patients receiving low-dose therapy. Typically, the a profound impact on patient management, it is adenopathy regresses 1 to 2 weeks after drug with- important to establish a ﬁrm diagnosis as soon as drawal. This begins with an understanding of the is an unusual manifestation of an adverse effect of clinical syndromes caused by various agents com- corticosteroids. Although mediastinal widening in bined with the prudent use of noninvasive studies patients receiving corticosteroids may raise the and invasive procedures. Legionella, and acid-fast bacteria stain and cul- Other rare pulmonary adverse drug effects ture); and (3) immunologic studies to exclude col- reported in the literature include busulfan-induced lagen vascular disorders and vasculitis. Long-term salicylate step in the evaluation of patients with localized or ingestion can cause a pseudosepsis syndrome diffuse pulmonary disease of unclear etiology. Differential Diagnosis of Radiographic Abnormalities Approach to the Patient With Suspected Drug-Induced Lung Disease Diffuse Disease Localized Disease Infection Infection Diferential Diagnosis Malignancy Malignancy Lymphangitic metastasis Pulmonary emboli As mentioned previously, the diagnosis of Pulmonary edema Radiation pneumonitis Pulmonary ﬁbrosis Drug toxicity drug-induced lung disease is one of exclusion Radiation pneumonitis/ﬁbrosis because there are no pathognomonic criteria. Mercapto- mended in patients for whom the diagnosis purine, the active metabolite of azathioprine, is an remains unclear and the differential diagnosis antineoplastic agent. These cytotoxic agents, which are unique in had histologic changes that could be attributed to their ability to cross the blood-brain barrier, are a drug reaction. Bleomycin accumulates against v 6 blocked bleomycin-induced ﬁbrosis in the skin and lung, resulting in skin ulcerations in mice, even when administered after the develop- and pulmonary ﬁbrosis. A disease-speciﬁc gene expres- monary damage, which is the major dose-limiting sion-proﬁling study in which the authors used side effect, was ﬁrst recognized in 1972. Patients typically present with a induced pulmonary toxicity centers on withdrawing subacute onset of a nonproductive cough and the drug and limiting exposure to exogenous oxy- dyspnea within a few weeks to 6 months after gen, as noted previously. Physical examination are generally administered to all patients with ﬁndings may show tachypnea, bibasilar crackles, clinically significant toxicity and then slowly and hyperpigmented skin lesions. Patients with bleomycin- induced hypersensitivity-type disease may have Busulfan, an alkylating agent that is used in the similar symptoms but often with an associated management of chronic myeloproliferative disor- fever, malaise, and chest radiographic changes of ders, was the ﬁrst chemotherapeutic agent impli- chronic pneumonitis and ground glass-appearing cated in causing chronic pneumonitis/pulmonary parenchyma with little ﬁbrosis. In general, alkylating agents (eg, busulfan, and pathologic distinctions between ﬁbrosis and cyclophosphamide, chlorambucil, and melphalan) pneumonitis are not always clear. The inci- total dose is 300 U but 20% when the total dose dence of symptomatic busulfan-induced pulmo- is 500 U18; however, pulmonary toxicity can occur nary ﬁbrosis is approximately 4 to 5%. Occasionally, more susceptible to bleomycin-induced pulmonary pleural effusions, nodular densities, or normal toxicity because of the fact that the kidneys primar- chest radiograph ﬁndings are noted.
A 48-hour review when estimating extent in the prehospital setting because erythema should be arranged for reassessment and simple low-adherent may develop into deeper burn within the ﬁrst 48 hours generic protonix 40 mg fast delivery. Minor burns to Burn extent can be difﬁcult to accurately assess close to the the face and scalp are best managed with application of petroleum- time of injury and the patient will be reassessed multiple times based jelly purchase 20 mg protonix mastercard, as occlusive dressings are not practical in these areas discount protonix 20 mg with amex. Cooling the burn, but not the patient Cooling provides good initial analgesia and may decrease the inﬂammatory response to injury. There is no strong evidence to Oral rehydration prove that early burn cooling will affect ﬁnal outcome. Care must be In the absence of other injuries, assuming the patient is able to drink taken to avoid cooling the patient overall, as evidence suggests and unlikely to require immediate surgery, then oral ﬂuids should mortality rates of burn victims increases with decreasing core body be commenced. The market is ﬂooded withahugevarietyofwounddressingsandthesevarygreatlyintheir The airway and burn injury (suspected characteristics and cost. Burns dressings in the acute setting need to inhalational injury) be simple, cheap and readily available. They need to start with of a low-adherent base layer that does not alter the clinical appearance There is often confusion over the terms airway burn and inhala- of the burn (which could affect further burn depth assessments). The two are distinct entities and should be managed Good examples include ClingFilm™, Seran wrap or petroleum accordingly. Alternatively for smaller burns, Mepitel a silicone-based dressing, may be useful. Because burns can Airway burns be associated with signiﬁcant ﬂuid leak, an absorptive layer such as Burns to the face, such as occurs during a ﬂash burn (Figure 18. This may also involve the upper airways (above the larynx) such Who needs ﬂuid resuscitation? During the ﬁrst 48 hours after burn injury, these areas are subject to signiﬁcant soft-tissue oedema, This differs between adults and children. In reality, Fluids are usually given intravenously and should be warmed to intubation can often be postponed until reaching hospital where minimize patient cooling. Typical ﬂuids are Hartmann’s, Ringers full anaesthetic and surgical support services are available. If prehospital deﬁnitive airway management is required: themselves from the contaminant by using gloves, eyewear and aprons. Ribbon tape Tissuedamageinelectricalburnsoccurssecondarytoheatgenerated or tube holders may be employed for short transfers, but may cut the face or lead to accidental extubation as the face swells. Resistance differs Inhalational injury according to tissue type with decreasing resistance seen going from Thermal injury to the lung and lower respiratory tract is rare due bone to skin to fat to nerve or muscle. Hence bone involvement to the excellent heat ﬁltering ability of the upper airway. However, can result in a signiﬁcant temperature rise with ongoing heat escape where a patient is exposed to the by-products of combustion such once the current has stopped. This results in signiﬁcant local tissue as carbon monoxide, carbon dioxide, cyanide, ammonia, sulphur, damage. Management of speciﬁc burns Fasciotomy and escharotomy Chemical burns Chemical burns will continue to destroy tissues until removed Escharotomy is an emergency procedure used in circumferential by irrigation or neutralization. Consequently, all liquid chemical burns where there is vascular compromise to the affected limb sec- burns require very thorough irrigation early (ideally within 10 ondary to a tourniquet effect of the burn in combination with tissue minutes of the burn) to limit tissue damage. Escharotomy involves making a longitudinal before irrigation and phosphorous must be kept damp otherwise it incision through the burned area in the limb or chest wall. Painand water (up to 1 hour) burning occur late • High-pressure steam • High-tension electrical Phosphorus burns Oxidizes to phosphorus Copious water irrigation, • Suspected non-accidental injury pentoxide. Particles of remove particles, apply • Large size >5% children 10% adults phosphorus can become copper sulphate, which embedded in the skin and can facilitate particle • Coexisting conditions, i. Bitumen Transported and used in Cool with copious liquid forms (Temperatures amounts of water • Burns may coexist with other trauma injuries. Burns are • High-risk environments for mass burns in particular include off- due to the high shore oil rigs, mines, nightclubs and enclosed spaces with public temperature rather than the toxic effects gatherings. Tar Burns by heat and phenol Treat by cooling and Recent examples include the Melbourne Bush Fires (2009 – 173 toxicity remove with toluene dead at scene), the Bali nightclub bombing (2002 – 411 casualties), Eye involvement Susceptible to damage due to Copious irrigation and the Piper Alpha oil-rig disaster (1988 – 228 casualties), the King’s thin ophthalmology referral Cross Underground ﬁre (1988 – 91 casualties), and the Bradford Football Stadium ﬁre (1982 – 256 casualties). The emergency response must be pre-planned and well commu- compartment and compartment syndrome and this may also be nicated to be effective. Patients with signiﬁcant burns irrespective of mechanism should • Expectant – in mass casualty situations, this group will include be referred to or taken to local accident and emergency depart- patients who might survive given individual and prompt care, but ments for further assessment and treatment. All resuscitation this patient type is ‘resource hungry’ and distracts from caring burns should go to a burns unit/centre either directly or for multiple other patients with better chances of survival. Burns 2000; unreliable, if there is any doubt treat judiciously and transport to a 26, 5:422–434. Emergency and early management of burns and • No international guidelines exist for advanced airway scalds.