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Administer a second analgesic as dificulty in ventilating her and agitation are secondary to poorly controlled pain buy 0.5mg avodart fast delivery medications causing hyponatremia. Propofol infsion syndrome is a rare but serious and potentiallyfatal adverse efect order avodart 0.5mg overnight delivery symptoms 10dpo, typically seen with infsion rates >83 lgfkg/min for more than 48 hours and carries with it a mortality rate of up to 85% buy avodart with a visa symptoms 3 dpo. This syndrome is charac­ terized by dysarrhythmias avodart 0.5mg on-line symptoms jaw pain and headache, heart failure, metabolic acidosis, hyperkalemia, and rhabdomyolysis. High-risk patients include those receiving high doses of the drug, those with history of hypertriglyceridemia, and those concurrently receiving parenteral lipids for nutrition. Treatment consists of immediate ces­ sation of propofol infsion and then correction of hemodynamic and meta­ bolic abnormalities. Some patients mayremaindelirious, agitated, andhave difculty maintain­ ing ventilation regardless of whether they are on an efective dose of anxio­ lytic drugs. Ifthe patient is tracheally intubated, mechanically ventilated, and receiving adequate sedation, using a neuromuscular blockade to paralyze the patient is a good option. Fentanyl is metabolized by the liver which creates inactive metabolites that are excreted by the kidneys. Because the metabolites are inactive, fentanyl a good choice for patients with renal insuficiency. Morphine is conjugated by the liver to metabolites that include morphine-6-glucuronide, a potent metabo­ lite. Both morphine and morphine-6-glucuronide are eliminated by thekidney, thus patients with renal dysfunction may sufer from prolonged drug efects. What are post-resuscitation treatment strategies that have shown to improve outcome? Other strat­ egies that have shown to improve neurologic outcome in post-cardiac arrest patients include controlled reoxygenation, therapeutic hypothermia, and glu­ cose management. To learn the post-cardiac arrest syndrome and strategies directed toward its management, including optimization of neurological outcome, optimization of myocardial fnction, glucose management, and controlled reoxygenation. Describe the use the therapeutic hypothermia to reduce the neurological injury after resuscitation. Maintaining oxygen satura­ tion in the 96% to 98% range also decreases post-resuscitation sequelae. While prior interventions attempted to more strictly control serum glucose levels, more recent evidence has found that moderate hyperglycemia correlates to better prognosis. For the subset of patients with return of spontaneous circulation following resuscitation, the prob­ ability of survival is significantly improved. Post-cardiac arrest syndrome describes a number of complex pathophysiologic pro­ cesses, which are grouped into 4 major categories: post-resuscitation brain injury, ischemia/reperfsion injuries, myocardial dysfnction, and persistence of the pre­ cipitating cause of the cardiac arrest. In addition to depressed levels of arousal, 10% to 40% of post-cardiac arrest patients develop seizure activities that have to be monitored and treated. Some experts have proposed applying this strategy more broadly to include patients with cardiac arrest from other causes; however, the beneficial efects in these groups have not been demonstrated. During hypothermia, magnesium, phosphate, potassium, and calcium should be replaced to higher end of normal values. The potential complications asso­ ciated with hypothermia include increased infections from leukocyte dysfnction, increased bleeding from platelet and clotting factors dysfnction, and arrhythmias (predominantly atrial fibrillation). Post,resuscitation myocardial dysfunction isa transient reduction inleft and right ventricular fnction that presents after cardiac arrest for up to 24 to 48 hours. Because the majority ofout-of-hospital cardiac arrests occur as the result of acute coronary syndrome, patients with successful resuscitation from out-of-hospital cardiac arrest should be considered for intervention. In2 addition, in a multicenter cohort study, it was observed that adult patients with non-trauma-related cardiac arrests had a mortality odds ratio of 1. Based on these principles and clinical evidence, the target oxygenation for this patient during resuscitation and immediately following resuscitation should be 94% to 98% saturation, and not higher. Fluids and Va sopressors The resuscitation ofpatients with hemodynamic instability from hemorrhagic shock and sepsis are discussed in detail in other sections of this book. The Surviving Sepsis Campaign is a multinational sponsored efort to standardize the approach to the early management of patients with sepsis and septic shock. Fluids and vasopressor support strategies have been well defined based on these eforts. Similarly, recent clinical observations from the casualty management during the ongoing military conficts in the Middle East have led to developments in the resuscitation ofpatients with hemorrhagic shock. What remains relatively undefined is management strate­ gies to minimize the harm associated the initial aggressive resuscitation of patients with sepsis, septic shock, and hemorrhagic shock. These fluid shifts produce edema and organ dysfnction, especially in the lungs and gastrointestinal tract. Resuscitation eforts directed at optimizing tissue oxygenation are most valuable during the initial few hours following the septic or hemorrhagic insults, whereas extended periods of excess fluid administration in these patients is potentially harmful. Strong eforts should be made to limit fluid administration; those who have had excessive fluids should receive timely diuretic treatment as soon as shock has been corrected. Early fluid restriction to avoid hypervolemia is associated with improved recovery from acute lung injury and acute respiratory distress syndrome. Glucose Levels Hyperglycemia is a common encounter in post-cardiac arrest patients. The 2010 American Heart Association Guidelines for Cardiopulmo­ nary Resuscitation and Emergency Cardiovascular Care now recommends moderate glycemic control targeting glucose values between 144 and 180 mgdL, to avoid possible hypoglycemia. Glycemic control does not play a role in the management ofpatients fol- lowing cardiac arrest. Therapeutic hypothermia to core temperatures of 32 C to 42 C for 24 to° ° 48 hours has been shown to improve neurological outcomes in patient following V-fib arrests. Cooling of patients to 28 C to 30 C is associated with increased° ° risk of arrhythmia without additional improvement in neurological outcomes. Even though maintaining euvolemia improves post-ardiac arrest patient outcomes, the use of Swan-Ganz catheter goal-directed therapy has not been proven to have survival benefits in these patients. Hyperglycemia and hypoglycemia are common following resuscitation from cardiac arrest and if unaddressed can contribute to worse neurological outcomes. Hypoglycemia in the post-resuscitation patient contributes to worsening neurological outcome; therefore, glucose­ containing solutions may be indicated if the patient is hypoglycemic. Resuscitation to achieve early hemodynamic goals (first 6 hours) has been shown to improve survival in septic patients; however, prolongation of resuscitation has not been shown to provide survival advantages. Intolerance to feeding, decreased pulmonary compliance, decreased oxygenation, and the development of abdominal compartment syndrome are associated with excess fluid administration and failure to reduce excess fluid administration following initial resuscitation from septic shock. Association between arterial hyperoxia following resuscita­ tion from cardiac arrest and in-hospital mortality. Therapeutic hypothermia after cardiac arrest in clinical practice: review and compilation of recent experiences. What are the possible complications related to his surgical disease processes, and how would you monitor and identif them? Management of fluid status: This patient needs cautious balance of his fuid status given his age and medical problems. Careful monitoring of urine output via Foley catheter and intravascular status with central venous pressure measurements will help guide management.

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Manual reduction of early postoperative strangulating hernia is risky given the fr iabilit y of the int est in es cheap avodart 0.5mg mastercard medicine hat jobs. N on op er at ive t r eat ment is n ot appr opr iat e wh en the cause of the small bowel obst ruct ion is most likely early post opera- tive fascial closure failure due to technical complications cheap avodart express symptoms 9f anxiety. This patient should be returned to the operating room for wound exploration discount avodart 0.5mg medicine januvia, inspection of the bowel and fascia order 0.5mg avodart fast delivery medications going generic in 2016, and reclosure of the wound. The woman described here underwent sigmoid colectomy for diverticular st rict ure. She developed a deep surgical sit e infect ion on post operat ive day 4, wh ich was t reat ed wit h opening of the skin wound and local wound care. Sev- eral days lat er she develops a small fascial defect wit h drainage of purulent fluid from this op en in g. To p u t it all t oget h er, sh e ap p ear s t o h ave a d eep su r gical sit e infect ion t hat caused a secondary deep surgical space infect ion (t hrough fascial erosion and ext ension of t he subcut aneous infect ious process); alt ernat ively, she may have had a deep surgical space infect ion t hat manifest ed init ially as a surgical sit e infect ion before spont aneously decompressing t hrough a fas- cial open ing. The prescribed regimen changes with anatomic source of the le a ka g e a n d ca n va ry b a se d o n the a n t ib io t ic su sce p t ib ilit y o f the o rg a n - ism s a t e a ch sp e cific t re a t m e n t fa cilit y. Durin g th e e valuation at th e h osp ital, h e was foun d to h ave fracture s of h is right femur, right radius and right ulna, and soft tissue contusions and abrasions on the right side of his body. The patient underwent open reduction and internal fixa t io n o f h is fe m u r fra ct u re a n d e xt e rn a l fixa t io n o f h is fo re a rm fra ct u re s wit h o u t any apparent complications. Th e p a t ie n t a p p e a rs a n xio u s and complains of having difficulty breathing and denies chest pain. Auscultation of the chest reveals diminished breath sounds bilaterally with scattered rhon- chi. Next steps: Ad m in ist r at ion of su p p lem en t al oxygen an d t r an sfer the patient t o the intensive care unit for close observation and possible mechanical ventila- tion if the condition deteriorates or does not improve. In addition, the pos- sibilit y of missed injuries such as int ra-abdominal hollow visceral injury needs to be considered. Direct blunt injuries to the lung parenchyma (pulmonary cont u sion ) can also cont r ibut e t o r espir at or y in su fficien cy. In a setting of recent trauma, it is also important to consider the possibility of missed injuries within the abdomen as the cause of his current respiratory insuf- ficiency. W ith these considerations in mind, our first priority for this patient is to address his respiratory insufficiency. Given t he significant t achypnea and t achycar- dia that this patient is demonstrating, it is very reasonable to consider intubation and mechanical vent ilation. The main reason for intubation is to help st abilize his respiratory status while we sort out the potential causes of his current problem. W hen the aspirated gast ric content s cont ain part iculate matter, bronchoscopy may be help- fu l t o h elp in clear in g the air way. Rou gh ly h alf of the patient s wit h aspir at ion event s will develop pneumonia; however, ant ibiot ics t reat ment is not indicat ed unless t he pneumonia develops. Incisional pain frequently affects the patient’s ability to clear air- way mucus, leading t o small airway obst ruct ion and ineffect ive bact eria clear- ance. Most commonly, nosocomial organisms colonize the pat ient s during t he hospitalization. The subsegment al at elect asis may progress to obstruction and inflammation, leading to larger airway obstruction and segment al collapse. The increase in the amount of intersti- tial water can cause compression of the bronchovascular structures and additional V/ Q mismatches and worsening hypoxia. Inju r y t o the ch est wall an d r ibs can lead t o impair ed br eat h - ing mechanics t hat range from splint ing secondary to pain t o disrupt ed mechanics secondary to a flail chest. This condition is worsened by chest wall injury pain, leading to atelectasis in the uninvolved lung. The patients generally have 2 2 decreased oxygen exchange in addition to decreased pulmonary compliance. Patho- logically, t h ere is injury t o the pulmonar y endot h elial cells wit h int ense inflam- matory responses. T hese changes manifest clinically as severe hypoxia, decreased pulmonary compliance, and increase in dead space ventilation. H igh-oxygen delivery to the lungs can cau se oxygen fr ee r ad ical for mat ion an d h yp er oxic inju r ies. The assessment of each patient should be directed at the patient’s current status, as well as toward the anticipated condi- tion of the patient. The inability to maintain PaO of 60 mm Hg or an oxygen 2 saturat ion of 91% wit h a supplement al nonrebreat hing O mask indicates signifi- 2 cant alveolar-ar t er ial (A-a) gr adient, su ggest in g that m ech an ical vent ilat ion sh ou ld be instituted. Hypoventilation can be recognized by hypercapnia and respiratory acidosis on an arterial blood gas. Hypoxemia is detected often on t he basis of pat ient’s subject ive respiratory complaint, low O saturation by pulse oximetry, and a low PaO on the 2 2 blood gas. It is important to keep in mind the diagnosis of hypoxemia or hypoventila- tion should be based on the clinical assessment and a combination of factors, and not be based on a single laboratory parameter or a pulse oximetry reading. The resultant cascade of events includes both cellular and humoral component s t hat produce an inhomogeneous pat t ern of lung injury. The inflammatory response involves activated polymorphonucleocytes, which gen- erat e oxygen free radicals, cyt okines, lipid mediat ors, and nit ric oxide. The comple- ment, kinin, coagulation, and fibrinolytic systems are also involved. Endothelial damage ensues with an increase in microvasculature permeability, leading to the accumulat ion of ext ravascular lung water, and result ing in diminished lung volume and decreased lung compliance. As the process progresses, lung compliance is fur- ther reduced due to sloughing of type I pneumocytes and a decrease in surfactant Figure 5–1. Ch e s t ra d io g ra p h y re ve a lin g the b ila t e ra l d e n s e p u lm o n a r y in filt ra t e s t yp ic a l o f a c u t e resp iratory disease syndrome. Later in the process, there is an increase in interst it ial edema, alveolar collapse, and lung consolidat ion. It sh ould be applied wit h caut ion in individuals with condit ions t hat are not readily correct able (such as atelect asis or fluid overload). The use of noninvasive vent ilatory support is associ- ated wit h an increase in aspirat ion event s and should not be used in pat ient s who are unable to cooperate or protect t heir airways effect ively. T his creat es a posit ive t r an spu lmon ar y pressur e that en sures in flat ion of the lungs. Exhalation is passive and occurs after the release of positive pressure in the ventila- tor circuit. The ventilator settings that are applied can be either volume controlled or pressure controlled. Hig h - Fr e q u e n c y Ve n t ila t io n High-frequencyventilationalsousesanendotrachealtubetofacilitategasexchange; however, it delivers very small tidal volumes on the order of 1 mL/ kg body weight at rates of 100 to 400 breat hs/ minute. T his vent ilatory mode has been shown to be beneficial for the support of infants with respiratory distress syndrome; however, the benefits of high-frequency ventilator support in adults are less clear. Ex t r a c o r p o r e a l Li f e Su p p o r t Cardiopulmonary bypass of extracorporeal life support uses a heart-lung machine to take over the patient’s respiratory and/ or cardiac functions.

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However cheap avodart 0.5 mg amex medicine 2, in the majority of cases cheap avodart 0.5mg with visa symptoms ringworm, there is vertebral artery involvement and pyramidal signs (hemiplegia) are present discount 0.5mg avodart free shipping treatment narcolepsy. Medial medullary syndrome: • It is due to occlusion of lower basilar artery or vertebral artery or one of its medial branches purchase avodart 0.5 mg free shipping kapous treatment. It is characterized by contralateral hemiplegia, which spares the face, contralateral loss of vibration and joint position sense, ipsilateral paralysis and wasting of tongue. A: As follows: • Cerebellar gait (Ataxic gait): Broad-based reeling or drunken gait. The patient walks with very short, shuffing and irregular steps with loss of associated movements. It is similar to that of Parkinson’s disease (except, there is no resting tremor, retained arm swinging, upright posture and wide based stance). Found in Sydenham’s chorea, Huntington’s disease and other forms of chorea, athetosis or dystonia. The patient is unable to walk, to stand, falls far to the side on walking but usually regains balance before hitting the ground. A: It is a type of gait adopted to avoid pain on weight bearing structures, characterized by very short steps with fxed leg posture. It is due to painful condition of joints (such as hip, knee, ankle) or injury to the bones or soft tissue. Presentation of a Case: • There is orofacial dyskinesia with chewing, pouting, lip smacking, grimacing, tongue movement associated with choreo-athetosis of the limbs and trunk. Tardive means after chronic exposure to dopamine receptor blockers (such as antipsychotic, antiemetic). Involuntary movements involve the tongue, lips, face, trunk and extremities that have persisted for at least 4 weeks and that began during treatment with neuroleptics or within 4 weeks of discon- tinuing neuroleptics. Presentation of a Case (Supposing Right Side): • There is wasting of anterior tibial and peroneal group of muscles on the right lower limb. My diagnosis is Right-sided foot drop (comment on caliper shoes or splint, if any). Foot drop (right) Foot drop (left) Unable to dorsiflex (right sided foot drop) Q:Where is the lesion? A: 2 branches: • Superfcial peroneal nerve: Sensory to lateral calf and dorsum of foot, also responsible for eversion of foot (motor). Deep peroneal nerve: Dorsifexion of foot and toe, sensation to the web space between 1st and • 2nd toes. A: In deep peroneal nerve palsy, the sensory defcit will be limited to the area between 1st and 2nd toes. A: I want to examine the gait, which is high stepping gait (the patient lifts his foot high to avoid drag- ging the forefoot and there is an audible ‘clop’ of the foot as he walks). A: The nerve is usually injured at the head of the fbula due to fracture or compression by a tourniquet or splint. A: As follows: • Trauma (to the nerve, fbular fracture, total knee arthroplasty or proximal tibial osteotomy). A: Nerve conduction study (shows local conduction block or slowing in the region of head of fbula). A: As follows: • Common peroneal nerve palsy • Charcot–Marie–Tooth disease mebooksfree. My diagnosis is Distal motor and sensory neuropathy, most likely Charcot–Marie–Tooth disease. If present, it is suggestive of trauma or fracture that may cause common peroneal nerve lesion. Inverted-champagne-bottle Pes cavus Pes cavus with clawing Claw hand with wasting appearance of toes of small muscles of hand Q:What else do you want to see? My diagnosis is Distal motor and sensory neuropathy, most likely Charcot–Marie–Tooth disease. A:The patient usually presents with foot deformities or gait disturbance in early childhood or early adult life. Slow progression leads to features of polyneuropathy with distal weakness and wasting that begins in leg, associated with distal sensory loss. Affected family members may have forme fruste with only pes cavus and absent ankle jerks. A: As follows: • Hereditary motor and sensory neuropathy type-I: There is demyelinating neuropathy. Posterior tibialis and peroneus longus antagonize these muscles resulting in pes cavus. Or, • Examine the upper limbs or perform the neurological examination of the upper limbs. Grip and release test: normally a patient can make a fst and release 20 times in 10 seconds. Dynamic Hoffman’s sign: snapping patients distal phalanx of middle fnger leads to spontaneous fexion of other fngers (Hoffman’s sign). If the sign is negative, it can be tested by fexion and extension of the neck, may become positive during the manoeuvre, which indicates cervical spondylotic myelopathy (Dynamic Hoffman’s sign). A: Cervical myelopathy is a condition caused by narrowing of spinal canal leading to compression of spinal cord. In many patients, the condition stabilizes or even improves without interven- tion. If progression results in sphincter dysfunction or pyramidal signs, surgical decompression should be considered. Others: Cholesteatoma, haemangioblastoma, granuloma, medulloblastoma, nasopharyngeal carcinoma, dermoid tumour, arachnoid cyst, basilar artery aneurysm, metastasis. A: It is a triangular subarachnoid space that lies between the anterior surface of the cerebellum and the lateral surface of the pons. Boundaries: • Anterior: posterior surface of petrous temporal bone, including internal acoustic meatus. Of these, rheumatoid hand is quite common and also a very popular short case, though other cases are also common. Most of the diagnoses are straightforward that can be easily diagnosed by looking at the patient or a particular part at a glance. It is frequently asked either to examine a particular part of the body or to look at a part for a spot diagnosis. However, even if asked to examine a particular part, examinee must look quickly from head to foot. During examination of joints, ‘always look, feel, move, measure and compare with the other side’. A: I want to examine the skin of other parts of the body (see below), also hands, legs. Face in systemic Flexion of fingers with skin change (typical Infarction at the tip of the fingers with sclerosis hands in systemic sclerosis) flexion contracture N. May be resorption, beaking of the nails (pseudoclubbing due to resorption) and amputation of fnger (may be). A: The following questions should be asked: • Do your fngers change colour on exposure to cold?

By noting the change in measured areas or volumes of the ventricle during diastole and during systole buy generic avodart 0.5 mg online symptoms 8 dpo, fractional area change or ejection fraction can be calculated order 0.5mg avodart otc medicine shoppe locations. In critical illness purchase avodart 0.5 mg without prescription medicine urinary tract infection, however buy avodart 0.5 mg low price symptoms you need glasses, factors such as increased pulmonary vascular resistance, left ventricular dysfnction, or marked fuid overload may alter the pressures routinely found in the right ventricle. An acute increase in right ventricular pressures leads to right ventricular dysfnction and if severe, right ventricular failure. Just as in the assessment of the left ventricle, echocardiography can assess the right ventricle qualitatively or quantitatively. Qualitative findings of right ventricular enlargement and septal "bulging" toward the left ventricle suggest severe right ventricular dysfnction. For quantitative measurements, image resolu­ tion must be adequate to assess chamber volumes and Doppler fow measurements. Whether clinicians are armed with basic skills and equipment or more advanced training with slightly more sophisticated equipment, bedside echocardiography ofers an accessible, noninvasive adjunct for diagnosis of unstable, critically ill patients. Volume status: Assessment of adequate resuscitation is crucial in the management of patients in shock. Echocardiography ofers several noninvasive options for assess­ ment of preload (ie, volume status). Equipment capable of measuring Doppler fow patterns can frther elucidate preload by measuring fow across the mitral valve and within the pulmonary artery. Like­ wise, echocardiographic assessment of left ventricular volumes during the cardiac cycle can estimate left ventricle preload by measuring left ventricular end diastolic volumes. Doppler technology can be used to measure fow across the left ventricular outflow tract to estimate cardiac output. Defects in the ventricular or atrial septum and valvular regurgitation can be visualized with fow Doppler. Increased fluid in the pericardium and its efect on filling of the ventricles during diastole will identif tamponade physiology if preload is compromised by the amount offluid in the pericardia! Additionally, therapy for cardiac tamponade can be initiated with ultrasound-guided pericardiocentesis. Source identification: When patients experience clinical decline, imaging plays a key role in identifying the source of the problem (see Table 6-3). These studies can be nonspecific and in the case of ultrasound, operator-dependent. Additionally, there are regions of the abdomen, mediastinum, and cranium that are dificult to image with portable ultrasound due to the density of adjacent structures, especially bone. Computed tomography offers a more sensitive and specific way to evaluate the brain, thorax, and abdo­ men. Whenthe acute decline is neurologic, noncontrast computed tomography is used to assess for intracranial pathology, such as worsening traumatic brain injuries, hem­ orrhagic stroke, or ischemia strokes. Patients who require mechanical ventilation, close monitoring, and frequent interventions are poor candidates for this diagnostic modality. Using an ultrasound to mark the vein position prior to applying sterile skin prep B. The respiratory therapist reports that she became more dificult to ventilate with the Ambu-bag (transport ventilation device). On your preliminary examination, she has absent breath sounds on the right and her respiratory rate is 34 breaths/minute and her oxygen saturations are now 87% with an increase to 100% inspired oxygen on the ventilator. On initial evaluation, he is unresponsive, his skin is ashen, extremities are cool, and he is perspiring. His blood pressure is 80/65 mm Hg, heart rate is 102 beats/minute, and he has distended neck veins. There are several trauma resuscita­ tions on other patients occurring simultaneously and you are given one choice of diagnostic machine to use (because all the equipment is being shared). He is fully resuscitated but remains on 2 vasopressor agents and has a mean arterial pressure of 72 mm Hg. A 43-year-old man on the ventilator with increased peak airway pressures, increased work of breathing, and diminished breath sounds on the left. Although thoracic computed tomog­ raphy can give valuable information on chest pathophysiology, the patient presented with acute respiratory decompensation and signs worrisome for right pneumothorax. Modalities such as bedside thoracic ultrasound to evaluate presence or absence of pleural sliding and portable chest radiograph (performed in a timely manner) could both identif a clinically significant pneumothorax. Right needle thoracostomy can be performed in patients in whom you have a high index of suspicion for pneumothorax. This procedure, when performed appropriately, is of relatively low risk and transient therapeutic benefit. Repeat­ ing auscultation once a room quiets down is quick, easy, and can help confirm presence or absence of breath sounds. The important point here is if a patient is unstable and diagnosis can be made at the bedside, it is safest not to transport the patient elsewhere for diagnostics. Clinical findings suggest cardiac dysfnction with severe malperfusion and distended neck veins. In the instance of tamponade, echocardiography can be used real-time for a safer method ofpericardiocentesis. Of the patients listed, the obese man with subcutaneous emphysema will likely be technically challenging for bedside ultrasound-guided drainage of his subhepatic abscess. His body habitus and the subcutaneous air will increase artifacts and lessen the safety of the ultrasound-guided technique. Patients "A, C, and E" all have suspected pulmonary diagnoses that can be evaluated with either portable radiographs or thoracic ultrasound. Patient "D" has a likely cardiac source for her symptoms and can be evaluated with bedside echocardiography. Estimation of cardiac output by noninvasive echocardio­ graphic techniques in critically ill subjects. Abandoning daily routine chest radiography in the intensive care unit: meta-analysis. Basic critical care echocardiography: validation of a curriculum dedi­ cated to noncardiologist residents. Life sup­ port should continue while striving to maintain physiologic and laboratory variables "within normal limits" to preserve organ integrity until procurement of the organ by the transplant team. Co nsiderations This unfortunate 25-year-old man sufered a motor vehicle and has been diagnosed as brain dead, presumably due to global and irreversible loss of brain stem func­ tion. This patient is a candidate to be an organ or tissue donor, which is identified based on prior wishes such as indicated in an advanced directive or an organ donor card, and based on discussion with the family. The declaration of brain death requires establishing the patient being in a coma and with no evidence ofbrain stem refexes (such as breathing independently, pupil reaction to light, eye movement, or arms and legs pulling away from noxious stimuli). A coordinated team approach is likewise optimal to help the family through the grieving process, working with the medical team, and communicating with the transplant team. Guidelines generally include optimizing cardiovascular and pulmonary fnction, fluid and elec­ trolyte balance, identification and treatment of infection, and the administration of hormones. The Donor Risk Index shows how these "fixed" criteria are interrelated with the variable criteria. Donor organs are infuenced by the prevailing systemic physiology (eg, oxygen delivery, blood electrolyte composition, regional and sys­ temic cytokines).

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