Case Study for Final Exam Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means "grave muscle weakness." With current therapies, however, most cases of myasthenia gravis are not as "grave" as the name implies. In fact, for the majority of individuals with myasthenia gravis, life expectancy is not lessened by the disorder.
The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected.
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction - the place where nerve cells connect with the muscles they control. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. Acetylcholine travels through the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction. In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. Individuals with seronegative myasthenia gravis have no antibodies at all to receptors for acetylcholine and muscle-specific kinase, which is involved in cell signaling and the formation of the neuromuscular junction. These antibodies are produced by the body's own immune system. Thus, myasthenia gravis is an autoimmune disease because the immune system - which normally protects the body from foreign organisms - mistakenly attacks itself.
The thymus gland, which lies in the upper chest area beneath the breastbone, plays an important role in the development of the immune system in early life. Its cells form a part of the body's normal immune system. The gland is somewhat large in infants, grows gradually until puberty, and then gets smaller and is replaced by fat with age. In adults with myasthenia gravis, the thymus gland is abnormal. It contains certain clusters of immune cells indicative of lymphoid hyperplasia - a condition usually found only in the spleen and lymph nodes during an active immune response. Some individuals with myasthenia gravis develop thymomas or tumors of the thymus gland. Generally thymomas are benign, but they can become malignant. The relationship between the thymus gland and myasthenia gravis is not yet fully understood. Scientists believe the thymus gland may give incorrect instructions to developing immune cells, ultimately resulting in autoimmunity and the production of the acetylcholine receptor antibodies, thereby setting the stage for the attack on neuromuscular transmission. Although myasthenia gravis may affect any voluntary muscle, muscles that control eye and eyelid movement, facial expression, and swallowing are most frequently affected. The onset of the disorder may be sudden. Symptoms often are not immediately recognized as myasthenia gravis.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in myasthenia gravis varies greatly among patients, ranging from a localized form, limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles - sometimes including those that control breathing - are affected. Symptoms, which vary in type and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision (diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, difficulty in swallowing and shortness of breath, and impaired speech (dysarthria). Myasthenia gravis occurs in all ethnic groups and both genders. It most commonly affects young adult women (under 40) and older men (over 60), but it can occur at any age. In neonatal myasthenia, the fetus may acquire immune proteins (antibodies) from a mother affected with myasthenia gravis. Generally, cases of neonatal myasthenia gravis are transient (temporary) and the child's symptoms usually disappear within 2-3 months after birth. Other children develop myasthenia gravis indistinguishable from adults. Myasthenia gravis in juveniles is common. Myasthenia gravis is not directly inherited nor is it contagious. Occasionally, the disease may occur in more than one member of the same family. Rarely, children may show signs of congenital myasthenia or congenital myasthenic syndrome. These are not autoimmune disorders, but are caused by defective genes that produce proteins in the acetylcholine receptor or in acetylcholinesterase. Unfortunately, a delay in diagnosis of one or two years is not unusual in cases of myasthenia gravis. Because weakness is a common symptom of many other disorders, the diagnosis is often missed in people who experience mild weakness or in those individuals whose weakness is restricted to only a few muscles. The first steps of diagnosing myasthenia gravis include a review of the individual's medical history, and physical and neurological examinations. The signs a physician must look for are impairment of eye movements or muscle weakness without any changes in the individual's ability to feel things. If the doctor suspects myasthenia gravis, several tests are available to confirm the diagnosis. A special blood test can detect the presence of immune molecules or acetylcholine receptor antibodies. Most patients with myasthenia gravis have abnormally elevated levels of these antibodies. However, antibodies may not be detected in patients with only ocular forms of the disease. Another test is called the edrophonium test. This approach requires the intravenous administration of edrophonium chloride or Tensilon(r), a drug that blocks the degradation (breakdown) of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. In people with myasthenia gravis involving the eye muscles, edrophonium chloride will briefly relieve weakness. Other methods to confirm the diagnosis include a version of nerve conduction study which tests for specific muscle "fatigue" by repetitive nerve stimulation. This test records weakening muscle responses when the nerves are repetitively stimulated. Repetitive stimulation of a nerve during a nerve conduction study may demonstrate decrements of the muscle action potential due to impaired nerve-to-muscle transmission. A different test called single fiber electromyography (EMG), in which single muscle fibers are stimulated by electrical impulses, can also detect impaired nerve-to-muscle transmission. EMG measures the electrical potential of muscle cells. Muscle fibers in myasthenia gravis, as well as other neuromuscular disorders, do not respond as well to repeated electrical stimulation compared to muscles from normal individuals. Computed tomography (CT) may be used to identify an abnormal thymus gland or the presence of a thymoma. A special examination called pulmonary function testing - which measures breathing strength - helps to predict whether respiration may fail and lead to a myasthenic crisis. Today, myasthenia gravis can be controlled. There are several therapies available to help reduce and improve muscle weakness. Medications used to treat the disorder include anticholinesterase agents such as neostigmine and pyridostigmine, which help improve neuromuscular transmission and increase muscle strength. Immunosuppressive drugs such as prednisone, cyclosporine, and azathioprine may also be used. These medications improve muscle strength by suppressing the production of abnormal antibodies. They must be used with careful medical follow up because they may cause major side effects.
Thymectomy, the surgical removal of the thymus gland (which often is abnormal in myasthenia gravis patients), reduces symptoms in more than 70 percent of patients without thymoma and may cure some individuals, possibly by re-balancing the immune system. Other therapies used to treat myasthenia gravis include plasmapheresis, a procedure in which abnormal antibodies are removed from the blood, and high-dose intravenous immune globulin, which temporarily (4-6 weeks) modifies the immune system and provides the body with normal antibodies from donated blood. These therapies may be used to help individuals during especially difficult periods of weakness. A neurologist will determine which treatment option is best for each individual depending on the severity of the weakness, which muscles are affected, and the individual's age and other associated medical problems. With treatment, the outlook for most patients with myasthenia gravis is bright: they will have significant improvement of their muscle weakness and they can expect to lead normal or nearly normal lives. Some cases of myasthenia gravis may go into remission temporarily and muscle weakness may disappear completely so that medications can be discontinued. Stable, long-lasting complete remissions are the goal of thymectomy. In a few cases, the severe weakness of myasthenia gravis may cause a crisis (respiratory failure). A myasthenic crisis occurs when the muscles that control breathing weaken to the point that ventilation is inadequate, creating a medical emergency and requiring a respirator for assisted ventilation. In patients whose respiratory muscles are weak, crises - which generally call for immediate medical attention - may be triggered by infection, fever, or an adverse reaction to medication Much has been learned about myasthenia gravis in recent years. Technological advances have led to more timely and accurate diagnosis, and new and enhanced therapies have improved management of the disorder. Much knowledge has been gained about the structure and function of the neuromuscular junction, the fundamental aspects of the thymus gland and of autoimmunity, and the disorder itself. Despite these advances, however, there is still much to learn. The ultimate goal of myasthenia gravis research is to increase scientific understanding of the disorder. Researchers are seeking to learn what causes the autoimmune response in myasthenia gravis, and to better define the relationship between the thymus gland and myasthenia gravis.

2. Priority care involves maintaining airway and C- spine immobilization, assessing for airway obstructions, respiratory rate and rhythm, depth and symmetry. A spinal cord injury must always be considered while performing any assessment. Careful evaluation of respiratory rate, chest wall expansion, abdominal wall movement, cough, and chest wall and or pulmonary injuries should be evaluated. Arterial blood gases and O2 saturation are essential because bedside diagnosis of hypoxia or carbon dioxide retention may be difficult. Assessment for circulation such as peripheral pulses and capillary refill time should be done to confirm tissue perfusion. Neurological checks should be performed. Complete vital sign assessment and diagnostic test such as CT scan to detect head, spinal or abdominal injuries and internal bleeding. Femur fracture should be immobilized, pedal pulse checks and bleeding controlled. Measures should be taken to minimize the risk of wound infection. Assess for signs of head injury and for signs of increased intracranial pressure. * Patient is with a femur fracture: Emergency care required: Fracture reduction and immobilization * Reduce fractures to near-anatomic alignment by using in-line traction. This reduces pain and helps prevent hematoma formation. Hold reduction by a traction device (i.e., Hare, Buck) or long-leg posterior splint. This is usually done by EMS personnel * Pneumatic splint may have additional benefits of reducing blood loss by direct pressure and tamponade of hematoma formation. Traction is often required to hold the femur out to length because of contraction of large muscle mass in the thigh. Immobilization also helps with pain control. * Pain management: Pain management is the most significant intervention of the emergency physician. Use parenteral opiate-type analgesics 9Morphine is most common) to the extent that respiratory and circulatory parameters allow. Intravenous administration allows for the most reliable titration to pain relief while providing ready access for reversal agents (i.e., Naloxone, Narcan) if necessary. * Infection prophylaxis: With open fractures, administer tetanus toxoid (unless given within 5 years) and use antibiotics with excellent staphylococcal coverage and good tissue penetration. Often, a first-generation cephalosporin (i.e., Cefazolin Sodium) is administered in combination with Gentamicin. New studies have shown that as long as antibiotics are given an open wound can withstand being open for up 24 hours without surgical intervention with a mild risk of infection. * Other: In addition to maintenance intravenous fluids, patients suspected of significant blood loss should be resuscitated with crystalloids (Lactated Ringers). Place a Foley catheter, and restrict all patients to taking nothing by mouth (NPO) until seen by an orthopedic surgeon.
3. No rectal tone is a sign of a C4-C5 fracture. The goal for this patient is to maintain C-spine immobilization to prevent further injury. Monitor the effects on the cardiovascular and respiratory systems. The clinical assessment of pulmonary function in acute spinal cord injury begins with careful history taking regarding respiratory symptoms and a review of the underlying cardiopulmonary co morbidity. A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction. With an injury at C-3 thru C-6, vital capacity is 20% of a normal uninjured person and their cough is weak and ineffective. In all patients, a complete detailed neurological assessment including motor function, sensory evaluation, deep tendon reflexes and perineal evaluation is critical. The presence or absence of sacral sparing is a key prognostic indicator.
The outcome of a patient can be associated with their best response in the first twenty-four hours after injury. Using the Glasgow Coma Scale (3 to 15, with 3 being a person in a coma with the lowest possible score, and 15 being a normal appearing person).This patient has a possible head injury and typically subdural hematomas are diagnosed with a CT scan. When one occurs in this way, it is called an "acute" subdural hematoma. Acute subdural hematomas are among the deadliest of all head injuries. The bleeding fills the brain between the actual brain tissue and the Dura very rapidly, compressing brain tissue and often causing a shift in the location of the brain and tissue death. Surgery is usually required as soon as possible to prevent any more brain damage or even death. With increase in blood pressure and decrease in heart rate this becomes more important. As the hematoma enlarges, it puts increasing pressure on the brain and causes neurological abnormalities including slurred speech, impaired gait and dizziness and can lead to coma or death. Diagnosis is made with CT or MRI. Treatment may range from watchful waiting in the case of a small epidural bleed to trepanation-drilling through the skull to drain the excess blood. The patient may also possible have a skull fracture. A basilar skull fracture is a fracture involving the base of the skull, typically involving the temporal bone, occipital bone, sphenoid, and/or Ethmoid bone. Often in this type of head injury the eardrum becomes ruptured and causes this seriosanginous drainage from the ear. These fractures can cause tears in the membrane surrounding the brain, or meninges, which results in the leakage of the cerebrospinal fluid. The leaking fluid may accumulate in the middle ear space, and dribble out through a perforated eardrum (CSF otorrhea) or into the nasopharynx via the Eustachian tube, causing a salty taste. CSF may also drip from the nose (CSF rhinorrhea) in fractures of the anterior skull base, yielding a halo sign. These signs are synonymous for basilar skull fractures. Bones may be broken around the foramen magnum, the hold in the base of the skull through which the spinal cord exits and becomes the brain stem, creating the risk that blood vessel and nerves exiting the hole may be damaged. Signs and symptoms of basilar skull fractures may include battle sign- ecchymosis of the mastoid process of the temporal bone, raccoon eyes- periorbital ecchymosis, cerebralspinal fluid rhinorrhea, cranial nerve palsy, bleeding from the nose or ears, hemotympanum, irregularities in vision and even death. These often heal without intervention but the patients are at risk of getting meningitis. The patient is at risk for abdominal injury with abdominal swelling and tightness. The patient could possibly have internal injuries or internal bleeding into the abdomen. Although protected under the bony ribcage, the spleen remains the most commonly affected organ in blunt injury to the abdomen in all age groups. Blunt injuries to the spleen are documented most frequently as the primary solid organ injury in the abdomen. These injuries are a common result from motor vehicle crashes, domestic violence, sporting events, and accidents involving bicycle handlebars. Hypotension in a patient with a suspected splenic injury, especially if young and previously healthy, is a grave sign and a surgical emergency. An injured spleen makes the abdomen painful and tender. Blood in the abdomen acts as an irritant and causes pain. The pain is in the left side of the abdomen just below the rib cage. Sometimes the pain is felt in the left shoulder. The abdominal muscles contract reflexively and feel rigid. If enough blood leaks out, blood pressure falls and people feel light-headed, have blurred vision and confusion, and lose consciousness (fainting).This should prompt immediate evaluation and intervention When surgery is necessary, usually the entire spleen is removed (splenectomy), but sometimes surgeons are able to repair a small tear..

4. The nurse’s responsibility in this case would be to take the family to a quiet and private area and explain the accident and what happen. She should explain that the patient had life threatening injuries that required immediate action in order to save the patient’s life. She should tell them that in situations like this, two physicians may consent for the patient to have surgery if a family member cannot be reached to give consent. The nurse at this time should also offer to have the physician who is taking care of the patient to talk with the family and to answer any questions the family may have that the nurse has not answered.
5. Nursing assessment at this time should be continuity to monitor ventilation to insure the ventilator is working properly, assessment of circulation and hypoxia. Patient should be monitored and vitals assessed regularly. Blood pressure is low and heart rate is high so fluid status should be evaluated as well as signs of any electrolyte imbalances. Patients with spinal cord injuries may require complete care and since this patient is on a ventilator all needs must be assessed as well as urinary and bowel movements. Communication will be impaired so assessment is a huge responsibility and liability. Patient should be assessed for signs of autonomic dysreflexia. Autonomic dysreflexia (AD) is a syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) above the splanchnic sympathetic outflow (T5-T6). This condition represents a medical emergency, so recognizing and treating the earliest signs and symptoms efficiently can avoid dangerous sequelae (a pathological condition resulting from a disease, injury, or other trauma) of elevated blood pressure. SCI patients, caregivers, and medical professionals must be knowledgeable about this syndrome and its management. A patient with autonomic dysreflexia (AD) may have 1 or more of the following findings on physical examination:
A sudden significant rise in systolic and diastolic blood pressures, usually associated with bradycardia, can appear. The normal systolic blood pressure for SCI above T6 is 90-110 mm Hg. Blood pressure 20-40 mm Hg above the reference range for such patients may be a sign of AD. Profuse sweating above the level of lesion, especially in the face, neck, and shoulders, may be noted, but it rarely occurs below the level of the lesion because of sympathetic cholinergic activity. Goose bumps above, or possibly below, the level of the lesion may be observed. Flushing of the skin above the level of the lesion, especially in the face, neck, and shoulders, frequently is noted. The patient may report blurred vision. Spots may appear in the patient's visual fields. Nasal congestion is common. No symptoms may be observed, despite elevated blood pressure.
Episodes of autonomic dysreflexia (AD) can be triggered by many potential causes. Essentially any painful, irritating, or even strong stimulus below the level of the injury can cause an episode of AD.
Assessment for increased intracranial pressure should be evaluated due to patient having a head injury. In general, symptoms and signs that suggests a rise in ICP including headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain and papilledema. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness. In addition, if there is displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and the Cushing’s triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern. Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Cheyne-Stokes respiration, in which breathing is rapid for a short period and then absent for a short period, occurs because of injury to the cerebral hemispheres or diencephalon. Hyperventilation can occur when the brain stem or tegmentum is damaged. Patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg (unless tissue shifts at the same time). Only when ICP exceeds 40–50 mmHg do CPP and cerebral perfusion decrease to a level that results in loss of consciousness. Any further elevations will lead to brain infarction and brain death. A swollen optic nerve is a reliable sign that ICP exists. Patients may not be able to state he is in pain but pain should be assessed.
There may be fluid and electrolyte imbalances in place due to blood loss or due to medications given to reduce intracranial edema such a Mannitol (which is a very powerful diuretic). Test should be done for suspected imbalances and ordered by the doctor

* Blood chemistries (to check electrolytes, especially sodium, potassium, and bicarbonate levels) * Urine specific gravity (a high specific gravity indicates significant dehydration) * BUN (blood urea nitrogen -- may be elevated with dehydration) * Creatinine (may be elevated with dehydration) * Complete blood count (CBC) to look for signs of concentrated blood * Dehydration is significant depletion of body water and, to varying degrees, electrolytes. Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree of dehydration progresses, tachycardia, hypotension, and shock. * Assess for signs of hemorrhagic shock due to amount of blood loss during surgery and from open femur fracture. Shock is a state of inadequate perfusion, which does not sustain the physiologic needs of organ tissues. Many conditions, including blood loss but also including nonhemorrhagic states such as dehydration, sepsis, impaired autoregulation, obstruction, decreased myocardial function, and loss of autonomic tone, may produce shock or shock like states.
In hemorrhagic shock, blood loss exceeds the body's ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma. Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen delivery (ie, DO2), and increased oxygen consumption (i.e., VO2) by tissues. Lactate levels, acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and co morbid factors all may affect a patient's response to hemorrhagic shock.
Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure.
Patient received blood. There is risk associated with blood transfusions. The nurse must assess the patient for these risks. There are risks associated with receiving a blood transfusion, and these must be balanced against the benefit which is expected. The most common adverse reaction to a blood transfusion is a febrile non-hemolytic transfusion reaction, which consists of a fever which resolves on its own and causes no lasting problems or side effects. Hemolytic reactions include chills, headache, backache, dyspnea, cyanosis, chest pain, tachycardia and hypotension. Blood products can rarely be contaminated with bacteria; the risk of severe bacterial infection and sepsis is estimated, as of 2002, at about 1 in 50,000 platelet transfusions, and 1 in 500,000 red blood cell transfusions. * Assessment of the abdominal incision for bleeding, edema, drainage (description), signs of wound dehiscence, signs of infection. This patient also had an open femur fracture. The femur is the largest and strongest bone and has a good blood supply. Because of this and its protective surrounding muscle, the shaft requires a large amount of force to fracture. Once a fracture does occur, this same protective musculature usually is the cause of displacement, which commonly occurs with femoral shaft fractures. * As with many orthopedic injuries, neurovascular complications and pain management are the most significant issues in patients who come to the ED. The rich blood supply, when disrupted, can result in significant bleeding. Open fractures have added potential for infection. Conduct a thorough examination to rule out associated injury. Hip fractures and ligamentous knee injuries commonly are observed in association. * At the site of fracture, tenderness on examination and visible deformity typically are noted. * The extremity may appear shortened, and crepitus may be noted with movement. * The thigh is often swollen secondary to hematoma formation. * Perform a thorough vascular examination on the extremity. Signs of vascular compromise should prompt arteriography and a vascular surgical consult. Physical signs of arterial injury include the following: * Expanding hematoma * Absent or diminished pulses * Progressive neurologic deficits in a closed fracture * Because of extensive blood supply to the musculature surrounding the femur, diaphyseal fractures may be associated with significant blood loss (i.e., 1 L or more) and resulting tachycardia and hypotension. * Test distal neurologic function, though examination is frequently unreliable because of the amount of pain associated with these fractures. Nerve injury is rare because of protective surrounding musculature. * Emergently consult an orthopedic surgeon-Evidence of vascular or progressing neurologic compromise should prompt emergent consultation with a vascular surgeon. In some hospitals, the general surgeon may have privileges for vascular intervention.

6. Pressure support ventilation is a method of assisting spontaneous breathing. It can be used as a partial or full support mode. The patient controls parts of the breath except the pressure limit. The patient triggers the ventilator and then ventilator delivers a flow up to a preset pressure limit. The purpose of Peep is to restore functional residual capacity for what is normal for the patient, when lung volumes are low. The presence of an endotracheal tube increases the resistance of inspiration, add to this a lung injury and the patient incurs a high workload of breathing. Pressure support offsets this work-it offloads the respiratory muscles in order to return the tidal volume to normal. The term pressure support ventilation describes the combination of pressure support and PEEP. Pressure support is used to assist spontaneous breaths in SIMV ventilation patient can be easily weaned using this technique, as the backup rate is withdrawn initially and then the pressure support. PEEP is pressure controlled ventilation and is frequently used in hypoxemic patients in acute respiratory failure. The principle method of controlling hypoxia is to increase airway pressure by prolonging inspiration. If CO2 is rising a physician may increase the respiratory rate in an attempt to reduce CO2.
Mechanical ventilation is often a life saving intervention but carries many potential complications including pneumothorax, airway injury, alveolar damage, and ventilator associated pneumonia. Assist Control is the mode the ventilator provided a mechanical breath with either a pre set tidal volume or peak pressure every time the patient initiates a breath. Traditional assist control used only a pre set tidal volume when a present peak pressure is used this is also sometimes termed intermittent positive pressure ventilation or IPPV. In most ventilators a back up minimum rate is set in case the patient becomes apnoeic. A maximum rate is usually not set but an alarm can be set if the ventilator cycles too frequently. This can alert that the patient is tachypneic.

7. With a falling PaO2 that is refractory to O2, ARDS should be suspected due to risk for infection, injury from trauma and mechanical ventilation. In both types of ARF, flooded airspaces allow no inspired gas to enter, so the blood perusing those alveoli remains at the mixed venous O2 content no matter how high the fractional inspired O2 (Fio2). This ensures constant admixture of deoxygenated blood into the pulmonary vein and hence arterial hypoxemia. In contrast, hypoxemia that results from ventilating alveoli that have less ventilation than perfusion (i.e., low ventilation-to-perfusion ratios as occurs in asthma or COPD and, to some extent, patients with ARDS/ALI) is readily corrected by supplemental O2. If supplemental O2 does not improve the O2 saturation to > 90%, right-to-left shunting of blood should be suspected. An obvious alveolar infiltrate on chest x-ray implicates alveolar flooding as the cause, rather than an intracardiac shunt. At the onset of illness, however, hypoxemia is often present before changes are seen on x-ray. Once AHRF is diagnosed, the cause must be determined, considering both pulmonary and extra pulmonary causes. , history is suggestive; pneumonia should be suspected in an immune compromised patient, and alveolar hemorrhage is suspected after bone marrow transplant or in a patient with a connective tissue disease. Frequently, however, critically ill patients have received a large volume of IV fluids for resuscitation, and high-pressure AHRF (i.e., caused by ventricular failure or fluid overload) resulting from treatment must be distinguished from an underlying low-pressure ARF (i.e., caused by sepsis or pneumonia).
High-pressure pulmonary edema is suggested by a 3rd heart sound, jugular venous distention, and peripheral edema on examination and by the presence of diffuse central infiltrates, cardiomegaly, and an abnormally wide vascular pedicle on chest x-ray. The diffuse, bilateral infiltrates of ALI/ARDS are generally more peripheral. Focal infiltrates are typically caused by lobar pneumonia, atelectasis, or lung contusion. Although echocardiography may show left ventricular dysfunction, implying a cardiac origin, this finding is not specific because sepsis can also reduce myocardial contractility.

When ALI/ARDS is diagnosed but the cause is not obvious (i.e., trauma, sepsis, severe pulmonary infection, pancreatitis), a review of drugs and recent diagnostic tests, procedures, and treatments may suggest an unrecognized cause, such as use of radiographic contrast agent, air embolism, or transfusion. When no predisposing cause can be uncovered, some recommend doing a bronchoscopy with bronchoalveolar lavage to exclude alveolar hemorrhage and eosinophilic pneumonia and, if this is not revealing, a lung biopsy to exclude other disorders (i.e., extrinsic allergic alveolitis, and acute interstitial pneumonitis). Barrow trauma is a well-recognized complication of mechanical ventilation. Although most frequently encountered in patients with the acute respiratory distress syndrome (ARDS), it can occur in any patient receiving mechanical ventilation. In clinical medicine, barrow trauma is used to describe the manifestations of extra-alveolar air during mechanical ventilation. Early descriptions of barrow trauma refer to rupture of the lung after forceful exhalation against a closed glottis, such as pulmonary injury after a deep-sea dive (i.e., breath-holding while pearl diving). Although nonmechanically ventilated patients may have barrow trauma, most cases occur in patients receiving mechanical ventilation.
The clinical presentation can vary, ranging from absent symptoms with the subtle radiographic findings of pulmonary interstitial emphysema (PIE) to respiratory distress or cardiac arrest due to a large tension pneumothorax. Other manifestations include subcutaneous emphysema, pneumopericardium, pneumomediastinum, and even pneumoperitoneum, singly or in combination. Barrow trauma was once the most frequent and easily recognized complication of mechanical ventilation. However, now evident is that barrow trauma represents only one of the mechanisms underlying the broad category of ventilator-induced lung injury (VILI). As the term suggests, the lung injury associated with barrow trauma is mediated by increased alveolar pressures. Other manifestations of VILI have been termed volutrauma, atelectotrauma, and biotrauma (cytokine and chemokine mediated) to reflect the major pathophysiologic events behind the injury.
Alveolar over distension is the key element in the development of barrow trauma. In this sense, barrow trauma is a misnomer because barrow trauma suggests the presence of elevated pressures in its pathogenesis. Current concepts suggest that high tidal volume ventilation produces the alveolar disruption that triggers this chain of events. The manifestations of barrow trauma span the entire clinical spectrum, from totally asymptomatic to full cardiac arrest. The severity of the presentation depends on the amount of extra-alveolar air present. In some individuals, the diagnosis is made only on the basis of chest radiographic findings.
Because patients usually cannot communicate because of intubation, signs of respiratory distress (i.e., tachypnea, patient-ventilator discoordination, use of accessory muscles [i.e, neck muscle], diaphoresis, tachycardia) may be the earliest indicators of barrow trauma.
Subcutaneous emphysema may be palpable as crepitus under the skin. This crepitus can be unilateral and focal or bilateral, it can occur over the chest wall or supraclavicular area, and it can expand up to the neck and face and down to involve most of the body. In rare cases, auscultation reveals a systolic crunching sound over the pericardium. This represents mediastinal air and is referred to as the Hamman crunch or Hamman sign. A flail chest may be observed in patients with trauma. Flail chest appears as paradoxical movements during the respiratory cycle and is due to rib fractures or separation from the costal cartilages in at least 2 places. It may increase the suggestion of an underlying pneumothorax due to trauma, which may be indistinguishable from a pneumothorax due to the barrow trauma of mechanical ventilation. Barrow trauma can manifest as a pneumothorax, with a tension pneumothorax being the most feared complication in mechanically ventilated patients. The continuous application of positive-pressure ventilation serves to perpetuate the passage of air into the extra-alveolar space, eventually causing a tension pneumothorax if untreated. In these patients, bedside detection of a pneumothorax can be difficult because of the noise from the equipment usually needed for mechanical ventilation. Decreased breath sounds on the affected side or the side of the pneumothorax is an initial finding. After tension develops, accumulating air displaces the mediastinum and associated structures away from the pneumothorax (contralateral). This process includes contralateral displacement of the trachea. These findings may be detected by placing a finger in the space between the trachea and neck strap muscles just above the sternal notch. The space should be equivalent, and deviation decreases the amount of space palpable. Chest-wall expansion on the side of the pneumothorax is preserved or hyper expanded. A totally collapsed lung reveals decreased breath sounds on the side of the collapse, but chest-wall excursion is diminished, and the trachea is deviated to the side of the collapse. The distinction is important if tube thoracostomy is considered without the benefit of a confirmatory chest radiograph.
Ventilator management and the adjustment of ventilator settings has been the focus of treatment in patients at risk for barrow trauma. This approach is based on recognition of the deleterious effects of alveolar over distension. It follows that avoiding or minimizing alveolar over distension is key to preventing barrow trauma. Cardiac arrest due to tension pneumothorax may be the clinical manifestation first recognized. Although any cardiac rhythm is possible, pulseless electrical activity in a mechanically ventilated patient should suggest tension pneumothorax. Evaluation for a possible tension pneumothorax can proceed as discussed above. Cyanosis reflecting profound hypoxemia may be another finding in this situation, but it may also reflect the patient's underlying respiratory condition.
Although barrow trauma focuses on the thorax, it can also adversely affect other organ systems, as follows: * Systemic gas embolism is the most dramatic extrathoracic manifestation of barotrauma. This occurs in the context of the described thoracic manifestations, including lung cysts and pneumothoraces. Effects include cerebral air embolism with infarcts, myocardial injury, and livido reticularis. Some speculate that other clinical findings, such changes in sensorium, seizures, and cardiac dysrhythmias without a clearly identified cause, may also be related to episodic systemic gas embolization. Fortunately, this complication is rare and preventable with a strategy of low tidal volume ventilation. * The increased intrathoracic pressures that occur in mechanically ventilated patients may affect venous drainage of extrathoracic sites. This increase can affect venous return from the brain and abdomen, a change that may be of concern when the pressures in these areas are already elevated (eg, from cerebral edema or abdominal compartment syndrome). This process provides another impetus to adopt a ventilator strategy (ie, low tidal volume) that translates into lowered intrathoracic pressures. Of course, barotrauma only worsens the pressures in the extrathoracic areas. If the pressures in these areas are monitored, a sudden increase may herald barotrauma as opposed to a problem in the area monitored.

8. A patient with only 10ml of urine output in a 7 hour period is at risk for fluid volume deficit or kidney failure. He is also at risk for electrolyte imbalances. Dehydration is not a disease but a condition characterized by the body's depletion of fluid (water). Dehydration may also be accompanied by salt (sodium, chloride), or another electrolyte imbalance in the body. If not treated, severe dehydration can lead to a lowering of the blood pressure and death. Dehydration commonly results from protracted vomiting, diarrhea, or an inadequate fluid intake over an extended period of time. Many disease processes may be accompanied by one or more of these symptoms. Signs of dehydration include; * Decreased urine output * Lethargy, sleeplessness, or confusion * Rapid pulse (> 100 BPM) * Faintness or fainting when standing * Inability to retain oral fluids * Dry mouth
Electrolytes play a vital role in maintaining homeostasis within the body. They help to regulate myocardial and neurological function, fluid balance, oxygen delivery, acid-base balance and much more. Electrolyte imbalances can develop by the following mechanisms: excessive ingestion; diminished elimination of an electrolyte; diminished ingestion or excessive elimination of an electrolyte. The most common cause of electrolyte disturbances is renal failure. The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium. Other electrolyte imbalances are less common, and often occur in conjunction with major electrolyte changes. A high blood sodium level means you have hypernatremia and is almost always due to dehydration without enough fluid intake. Symptoms include dry mucous membranes, thirst, agitation, restlessness, acting irrationally, and coma or convulsions if levels rise extremely high. Increased potassium levels indicate hyperkalemia. Increased levels may also indicate the following health conditions: acute or chronic kidney failure, Addison's disease ,hypoaldosteronism , injury to tissue, infection, diabetes ,dehydration, excessive dietary potassium intake (for example, fruits are particularly high in potassium, so excessive intake of fruits or juices may contribute to high potassium),excessive intravenous potassium intake. Certain drugs can also cause hyperkalemia in a small percent of patients. Among them are non-steroidal anti-inflammatory drugs (such as Advil, Motrin, and Nuprin); beta blockers (such as propanolol and atenolol), angiotensin-converting enzyme inhibitors (such as captopril, enalapril, and lisinopril), and potassium-sparing diuretics (such as triamterene, amiloride, and spironolactone).
Possible acute renal failure due to reduced blood supply during surgery and damage to the right renal artery. Rapid time course (less than 48 hours)
Reduction of kidney function will show: * Rise in serum creatinine * Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μmol/l) * Percentage increase in serum creatinine of ≥50% * Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours
Acute kidney failure is the sudden loss of your kidneys' ability to perform their main function — eliminate excess fluid and electrolytes as well as waste material from your blood. When your kidneys lose their filtering ability, dangerous levels of fluid, electrolytes and waste accumulate in your body. Acute kidney failure is most common in people who are already hospitalized, particularly people who need intensive care. Acute kidney failure tends to occur after complicated surgery, after a severe injury or when blood flow to your kidneys is disrupted. Acute kidney failure can be serious and generally requires intensive treatment. However, acute kidney failure may be reversible. If you're otherwise in good health, you can recover normal kidney function.
When signs and symptoms point to acute kidney failure, blood and urine tests pin down the diagnosis. Changes associated with acute kidney failure include: * Daily urine output usually falls to less than 2 cups (500 milliliters). * Blood urea and creatinine levels rise rapidly. * Blood electrolyte concentrations — levels of minerals such as sodium, potassium and calcium that regulate fluid balance and muscle function, plus many other vital processes — become unstable, causing swelling (edema) and lung congestion.
Blood potassium, in particular, rises rapidly, often to life-threatening levels.

9. This patient is going to have several needs once he is off of the ventilator. Patient should be encouraged to cough and deep breathe. He should also be encouraged to use the incentive spirometer. Pillows should be used to help hold position. The spinal cord injury is going to leave the patient with full head and neck movement depending on muscle strength limited shoulder movement. Complete paralysis of the body and legs is present. The patient has no finger, wrist or elbow flexion or extension. Sympathetic nervous system will be compromised and there is a possibility of autonomic dysreflexia. The patient could benefit from the use of an electric wheelchair that may be controlled by either a chin or sip and puff controller but this will vary depending on dexterity. The person will require total assistance when transferring from a bed to a wheelchair and from a wheelchair into a car. A hoist will have to be used, possibly by two assistants for safety. Complete assistance will be required during mealtimes. The patient will be able to breathe without a ventilator using diaphragm. Assistance required to clear secretions and assistance in coughing will be required. Complete personal assistance is required. The person will need assistance with washing, dressing, and assistance with bowel and bladder management. A computer may be operated using iris recognition. Patients with spinal cord injuries usually have permanent and often devastating neurologic deficits and disability. It is important to refer this patient to physical therapy, occupational therapy, and psychological therapy.