Sample Case Study The patient was a 77-year-old female who arrived to the emergency room on February 25 th with a chief complaint of shortness of breath and a deteriorating pulmonary status along with lower extremity weakness. The patient stated that several days prior to admission she started noticing some limitations and dyspnea. The patient lived alone, had a smoking history of 22 pack years, and quit smoking 17 years ago. She had a history of ethanol abuse in the past but has not been using alcohol for fifteen years and she attended Alcoholics Anonymous meetings. The patient s allergies included prednisone (a steroid) and Paxil (an antidepressant), and she was intolerant to augmentin (an antibiotic) and ultram (an analgesic). Her past medical history was significant for hypertension, osteoarthritis, hyperlipidemia, chronic gastroesophogeal reflux disease, an appendectomy and cholecystectomy. The patient also had a spontaneous pneumothorax in the past which resolved through reabsorption. Her family history was noncontributory. The patient was recently admitted to the hospital on February 2 nd with communityacquired pneumonia. She was treated, improved and sent home six days later. The patient presented to the emergency room on the 25 th of February in a very agitated state. Her blood gas on room air revealed the following: ph of 7.68, PO2 128 mmhg, PCO2 of 16.7 mmhg, HCO3-25 meq/l - interpreted as an uncompensated respiratory alkalosis. Her white blood cell count was 7.9 k/µl (normal), hemoglobin 15.2 g/dl (normal), and hematocrit of 47%(normal). A chest x-ray was taken and showed a faint infiltrate in the right upper lobe, which was likely seen because of her recent pneumonia. The admitting physician s initial
impressions upon arrival included dyspnea, possible pulmonary thromboembolism (PTE), possible pericarditis, and chest pain, which could be pleuritic in origin. A CT scan was done to rule out the PTE and an echocardiogram was done to determine possible pericarditis. The echocardiogram showed mild left ventricular hypertrophy with an overall normal left ventricular systolic function and possible diastolic dysfunction. An initial aerosol treatment was given using a bronchodilator (Duoneb ; 0.5 ml of Ventolin - albuterol/2.5 ml of Atrovent - ipratropium). The patient had bilateral decreased breath sounds, a heart rate of 98 beats per minute, and a respiratory rate of 25 breaths/min. She was also placed on two liters of oxygen via a nasal cannula with her SpO2 resulting at 98%. The following day she was weaned off of oxygen therapy to room air and the SpaO2 remained at 98%. On day three a pulmonary function test was done. The patient had a predicted forced vital capacity (FVC) of 3.09 liters and her measured FVC was 2.02 liters, giving her a 65 percent predicted FVC. Her forced expiratory volume in one second (FEV1) was predicted to be 2.27 liters and she achieved 1.40 liters, giving her a 62 percent predicted FEV1. Both of these are abnormally low (below 80% predicted). Her FEV1% was 69 also abnormally low. The patient showed no significant change after receiving Duoneb, a bronchodilator. Her peak expiratory flow was 71 percent predicted and her lung volumes were all proportionally decreased. The patient s diffusing capacity was 47 percent predicted and when it was corrected for the amount of alveolar ventilation, the value changed to 102 percent predicted. This showed that the patient did not have a diffusion problem. The interpretation of the pulmonary function test was that there was minimal
obstructive lung defect and a moderate restrictive lung defect. Also the test showed that the patient had an insignificant response to a bronchodilator. Over the next few days the patient s status remained relatively stable. On day five the impression of the patient was that she had developed lower extremity weakness. A neurologic exam was done. Results showed that the patient s speech and language were normal. Her motor strength was 10/10 in both upper extremities. When asked, the patient would not flex her knees or lift either foot off the bed. A sensory exam of her lower extremities showed that they were intact. Her SpO2 was measured to be 88% so the patient was put back on a nasal cannula at one liter per minute and showed an oxygen saturation of 94%. The impression of the patient was that she had Guillain-Barré Syndrome (GBS) and needed to be monitored for possible ventilatory failure. Bedside spirometry was ordered BID (twice a day) to monitor her pulmonary status. The patient s FVC was measured on day 5 was 1,050 and 1,290 milliliters (predicted FVC being 3.09 liters.) An ABG was obtained and analyzed with the following results: ph 7.52/PaCO2 32.5 mmhg/pao2 109 mmhg/ HCO3 22.8 meq/l (interpreted as an uncompensated respiratory alkalosis). Over the next 3 days her condition remained stable with FVC measurements ranging from 1,010 ml to 1,280 ml. During this time, with regards to the status of her GBS, the patient could not move her lower extremities on command but said she could feel it when the physical therapist touched her hands and that they were sensitive to touch. She received aerosol treatments with Duoneb QID and PRN at night. She had a weak, nonproductive cough for most of the time, and required oxygen therapy by nasal
cannula ranging from 1 to 4 L/min to keep her SpO2 above 92% (physician order this to be a goal). From day 9 to day 18 of her admission her FVC gradually improved and her strength began to return to her extremities. (FVC on day 14 was 1,680 ml and day 18 was 1,890 ml. FVC monitoring was discontinued on day 18). She continued to receive care as this case report ended. In overview, the patient, a 77-year-old female, was admitted to the hospital on February 25 th, 2009 with dyspnea and lower extremity weakness. Since her admission she continued to deteriorate and was diagnosed with Guillain-Barré Syndrome. Her respiratory status reached a low point but she did not require mechanical ventilation. She received oxygen therapy to maintain a SpO2 above 92% and she received Duoneb aerosol treatments QID and PRN at night to reduce her work of breathing, enhance her cough, and maximize her airflow/ventilation. The paralysis began improving as this case ended and she is expected to have a full recovery if all goes well.
Mehta, S. Neuromuscular Disease Causing Acute Respiratory Failure. Resp. Care 2006; 51(9): 1016-1021 The article I have chosen to summarize is about neuromuscular disease causing acute respiratory failure. It addresses the mechanisms underlying acute respiratory failure, clinical assessment for impending respiratory failure, predictors for the need for mechanical ventilation, noninvasive positive pressure ventilation, intubation and mechanical ventilation, weaning and extubation, and ICU morbidity and mortality. The article focuses on two neuromuscular diseases in particular: Guillain- Barré syndrome and myasthenia gravis. These two diseases are what account for a majority of acute respiratory failure associated with neuromuscular disease. There are four basic mechanisms that underlie acute respiratory failure and they include upper-airway compromise due to weakness of facial and neck muscles; weakness of the muscles of inspiration resulting in inadequate lung expansion, atelectasis, V/Q mismatch, and hypoxemia; expiratory muscle weakness prevents adequate cough and removal of secretions; and finally complications of the acute illness such as pneumonia. General warning signs for impending respiratory failure in patients with a neuromuscular disease include increasing generalized weakness, dysphagia, dysphonia, and dyspnea on exertion and at rest. A subjective assessment includes rapid shallow breathing, tachycardia, accessory muscle use, orthopnea, and cough after swallowing. Objective variables used to assess impending respiratory failure
include measurements of vital capacity, maximum inspiratory pressure, and maximum expiratory pressure. A vital capacity of 15 ml/kg or 1 L is generally accepted as an absolute criterion for intubation. With regards to noninvasive positive pressure ventilation, there is insufficient data to recommend its use in patients with neuromuscular disease. It may not be appropriate in patients with Guillain-Barré syndrome if a long duration of mechanical ventilation is anticipated. Between 25% and 50% of Guillain-Barré syndrome patients require intubation and mechanical ventilation, whereas 15-27% of myasthenia gravis patients require it. Complications of prolonged intubation include infections, aspiration, and atelectasis. The decision to extubate patients with neuromuscular disease can be a challenging one, especially in patients with myasthenia gravis whose condition fluctuates. In general, these patients should have an adequate cough, few secretions, and should tolerate a low level of pressure support for a prolonged period of time. This article relates to my case study because of the fact that the patient I followed was diagnosed with Guillain-Barré syndrome. Because of her disease her muscles began to weaken but she was still able to maintain adequate ventilation. She needed extensive work with physical therapy but is expected to recover and do well.