Abstract: To analyze the common lessons learned that lead to deterioration and death of patients during the recovery period of acute cerebrovascular disease. METHODS: A retrospective analysis was used to analyze the causes of death of 26 inpatients who died during the recovery period between 1996 and 2003. RESULTS: The common causes of death in the recovery period were significantly different from those in the acute phase and were mostly related to medical negligence. Conclusion: The common risk factors for death in the recovery period should be fully understood, and active prevention and early management can effectively reduce the occurrence of death.
The mortality rate of acute cerebrovascular didease (ACVD) is high, and the analysis of the causes of death in ACVD at home and abroad is mostly focused on the acute phase, but the causes of death in the recovery phase are rarely reported. From 1996 to 2003, there were 282 deaths of ACVD inpatients in our hospital, among which there were 26 deaths in the recovery period, accounting for about 9.22% of the deaths. The negative impact of death in the recovery period is even greater because the medical and nursing staffs and patients’ families are not fully prepared. Now we analyze these 26 cases in order to summarize the experience and lessons learned.
1.Clinical data
1.1, general information
Among the 26 cases in the group, 15 were male and 11 were female. The age ranged from 59 to 82 years old, with a mean age of 68.7 years old, of which 18 cases were over 65 years old. There were 19 cases with a history of hypertension, 3 cases each with a history of coronary heart disease and diabetes mellitus, 2 cases with a history of stroke, and 2 cases with chronic bronchial emphysema. Due to the long and recurrent course of the disease, the disease course was artificially divided into 3 periods: acute, recovery and post deterioration. Among them, the time from onset to stabilization followed by deterioration ranged from 13 to 48 days, with an average of 21.8 days, and the average time from onset to death was 24.3 days.
1.2, Symptoms and signs
Neurological conditions: 5 cases had mild disorders of consciousness (drowsiness to somnolence) on admission; 7 cases had muscle strength grade 2, 6 cases had grade I, 4 cases had grade II, 5 cases had grade III, 3 cases had grade IV, 1 case had grade V, and 5 cases had ball palsy. After treatment, each patient showed a more obvious improvement, and all of those with consciousness disorders regained consciousness; muscle strength improved by more than 2 levels on average. Those with ball palsy all resumed eating on their own. Internal medicine: 5 cases of fever, 4 cases of pulmonary infection, 8 cases of high blood pressure, 7 cases of high blood glucose, 5 cases of mild ECG abnormalities (low voltage in limb leads, atrial fibrillation, sinus bradycardia, ST-T changes, etc.), and 1 case of impaired renal function were present on admission. After treatment, fever, pulmonary infection and hypertension were well controlled. For those with high blood glucose, all of them returned to normal except for one case whose blood glucose still fluctuated significantly.
1.3. Imaging and laboratory tests
Twenty-five cases had fresh lesions on cranial CT at admission, including 6 cases of cerebral hemorrhage (5 cases with lesions in the basal ganglia region and 1 case in the parietal lobe, of which 2 cases broke into the ventricles) and 19 cases of cerebral infarction (7 cases with lesions in the cortex and 11 cases in the basal ganglia region, of which 4 cases had larger cerebral infarction and 2 cases had lacunar cerebral infarction; no lesions were found in I case, which was considered as reversible cerebral impairment (RIND) in combination with clinical considerations. 6 cases of cerebral hemorrhage After the condition was alleviated by treatment, the cranial CT was reexamined and the lesions were found to be significantly reduced.
There were 8 cases with increased leukocytes [(10.08~14.5)×109/L] in the acute phase, only 1 case with increased leukocytes in the recovery phase, and 9 cases with increased leukocytes after deterioration. 7 cases with increased blood glucose (8.9~22.5 mmol/L) in the acute phase, only 1 case with increased blood glucose in the recovery phase, and 8 cases with increased blood glucose (14.9~67.8 mmol/L) after deterioration. Blood potassium decreased in 1 case each in the acute and recovery periods, and decreased in 6 cases after deterioration (2.2~2.7 mmol/L).
2. Results
The causes of death in this group of 26 patients in the recovery period were mainly cardiovascular system complications (12 cases), secondary infections (5 cases), food asphyxia and aspiration pneumonia (5 cases), diabetic ketoacidosis or hyperosmolar coma (2 cases), malnutrition hypogammaglobulinemia (1 case), and trauma (1 case), etc. Eight of the 26 patients developed multiple organ failure after deterioration.
2.1, Myocardial infarction and arrhythmia
Five patients died of acute myocardial infarction (AMI), among which three cases were found to have mild abnormalities on ECG examination at admission, one case had slightly high cardiac enzymes at admission, two cases had several episodes of transient chest tightness or chest pain and cold sweats during the course of the disease, and one case had a sudden myocardial infarction after one week of constipation when the anal saixelu was in place; among the seven patients with arrhythmias, one case had low voltage in the ECG limb leads at admission, and six cases had low electropotassium (all below 3.5 mmol/L, lowest 2.8 mmol/L), and 2 cases of acidosis (TCO2 < 12 mmol/L = both patients had acute enteritis with diarrhea for several days before deterioration and already had acidotic conditions).
2.2, Pulmonary infection and aspiration pneumonia
Five patients died of pulmonary infection and its resulting serious complications, including three cases of infectious shock and two cases of diffuse intravascular coagulation (DIC), which were not significantly increased before the deterioration of the disease, but the blood examination already had a significant increase in leukocytes and an increased proportion of neutrophils, and had symptoms such as cough, poor appetite, and mental fatigue, etc. In three cases, shortness of breath and dyspnea were obvious when the disease worsened, and both lungs could be heard In two cases of DIC, the condition changed suddenly, with low blood pressure, skin petechiae, dramatic decrease in hemoglobin and hemoglobin, and a decrease in red blood cell pressure product to below 0.10. The blood was not coagulated, and in one case, an emergency cranial CT showed extensive hypodense lesions in the whole brain.
Five patients died of food asphyxia and complications and complications of aspiration pneumonia. Four of them had different degrees of bulbar palsy after the onset of the disease, but all of them had eaten by themselves (one of them had a gastric tube for 1 week), and one patient without bulbar palsy was lying down after eating, resulting in accidental aspiration of food reflux into the lungs.
2.3, Diabetes mellitus and other causes
Two patients died of diabetic ketoacidosis and hyperosmolar coma. These two patients had a history of diabetes mellitus, one had good control of blood glucose at one time, but hypertonicity occurred due to prolonged dehydration and excessive sugar supplementation, the other patient had slightly higher blood glucose on admission, but did not pay enough attention to it, and there were no targeted measures for diet, rehydration and dehydration; after diabetic ketosis and hyperosmolar coma (at that time, blood glucose was 2.57 mmol/ L, blood sodium 179 mmol/L, BUN 21.43 mmol/L, osmolality 389 mmol/L), dialysis treatment was administered, and the following day, bilateral pupils were unequal in size, and death was due to brain herniation.
One case probably died of hypovolemic shock, which was caused by severe malnutrition after the onset of the disease due to low food intake and inadequate intravenous nutrition, with blood biochemistry showing anemia, hyponatremia, hypogammaglobulinemia, gradual decrease in blood pressure, slowed heart rhythm, and finally death by failure.
One patient fell while practicing walking alone, resulting in femur fracture, followed by fever and multi-organ failure.
3.Discussion
In this group of 26 ACVD patients, the cause of death was not the common brain failure, brain herniation, or acute complication of multi-organ failure, but the deterioration of the disease and death when the brain damage had been obviously recovered and the systemic condition was stable, which occurred suddenly and was unexpected.
Patients with ACVD are of advanced age and often have hypertension, heart disease, diabetes mellitus, chronic lung disease, and a history of previous stroke, among which hypertension is the most common, because the disease is a systemic vascular disease, and important organs such as heart, kidney and brain are often involved. During the period of stable disease, there may be no obvious clinical signs, but once the body receives some kind of blow (such as asphyxia, fall, constipation, anal cycloid, etc.), the organs are prone to loss of compensation, or even functional failure and fatal soon, as a clinician, should be fully aware of this. At the same time, for some early signs of organ damage, even if they are mild and atypical (for example, cough, lethargy, abnormal blood picture, etc.), we should pay great attention to them and strive for early detection and early treatment.
Patients who are hospitalized have a significantly higher chance of in-hospital infection. Therefore, for patients who are already in the rehabilitation period, they should try to shorten their hospital stay and be discharged from the hospital for community rehabilitation or transferred to a rehabilitation unit for treatment as soon as possible. In addition, also because of the low immune function of the elderly, once the infection occurs, the clinical manifestations are often atypical, and the increase in fever and blood leukocytes is not always proportional, so it is easy to be overlooked, and when it becomes serious enough for infectious shock or DIC to appear, it is often too late for treatment. Therefore, for elderly patients with infections, anti-infective measures should be decisive and strengthened in a timely manner.
Elderly patients have poor absorption and metabolic capacity and are prone to disorders of water, electrolytes, acid-base balance and malnutrition, the presence of which may have no obvious clinical signs but is highly likely to cause arrhythmias, especially ventricular fibrillation. In addition, the presence of acidosis can cause damage in many ways, especially arrhythmias. Therefore, disorders of water, electrolytes, acid-base balance and malnutrition must be corrected early.
In patients with manifestations of bulbar palsy, the gastric tube should be left in place as soon as possible, and the nasal feeding should be kept in quality, and the tube should not be removed prematurely. On the one hand, the gastric tube can provide adequate nutrition to patients with dietary difficulties, and on the other hand, it can prevent food from being accidentally inhaled into the lungs and causing aspiration pneumonia. In addition, the head of the bed should be elevated 30°~45° when ACVD patients are nasal feeding or eating, and it is better not to lie down immediately after eating, or the head of the bed should be elevated 30° when lying down, and avoid turning the patient too early, which can prevent the regurgitation of food in the stomach into the stomach. If available, continuous gastric tube drip can be injected with intestinal nutrition such as Neng, which can prevent malnutrition.
For patients with diabetes mellitus, blood glucose changes must be detected frequently, and diet and rehydration should be limited to sugar intake as much as possible. Dehydrating agents should be applied carefully and cautiously. At the same time, adequate blood volume should be maintained to prevent blood concentration. In addition, for patients with ACVD, dialysis indications should be strictly controlled to avoid aggravating cerebral edema or triggering cerebral hemorrhage as a result.