Successful treatment of myocardial infarction of left main trunk by emergent CABG under IABP and PCPS support

We experienced a successful treatment of acute myocardial infarction which was due to left main trunk obstruction. A 54-year-old man with no history of angina was transported by a rescue squad in cardiogenic shock, and diagnosed by electrocardiography with a wide range of myocardial infarction. Emergent coronary arteriography was performed under IABP support, revealing 99% stenosis in the left main trunk. Percutaneous transluminal coronary recanalization (PTCR) was performed, but suddenly cardiac arrest was happened. He was put on emergency percutaneous cardiopulmonary support (PCPS). A Palmaz-Schatz stent was implanted for reperfusion, but the patient was hemodynamically unstable with frequent ventricular arrhythmia and pulmonary edema. 24 hours later he underwent coronary artery bypass grafting and CPB could be terminated intraoperatively. His cardiac function was very low and LVEF was 20%. All grafts were patent. On the rehabilitation he was discharged on postoperative day 162 and has returned to work in his office one year postoperatively.     

Therapeutic objectives and strategies in NBIA 1 (Hallovorden-Spatz syndrome)

A 10 years old male patient, DG, was admitted in the ICU because of continuous uncontrolled movements due to a neurologycal degenerative disease (Hallervorden-Spatz syndrome) able to determine reduction of spontaneous breathing efficacy. At admission he presented acute ventilatory failure, because of a Staphylococcus aureus broncopneumonia, so he had a tracheal tube and mechanical ventilation (pressure support). During hospitalization (4 months in ICU and 2 months in Pediatric Department) DG received tracheotomy and percutaneous gastrostomy, to obtain adequate spontaneous ventilation and artificial enteral nutrition; a satisfactory pharmacological control of choreo-athetosic movements, with not great interference with original sleep-awake cycle, was obtained. Actually DG is living in his family (9 months follow-up); he has tracheotomy and percutaneous gastrostomy; he can relate with the environment; in a few months, he'll go to school again. He need 30 daily administrations of 8 different drugs; family, supported by an integrated multidisciplinary équipe, takes care of him. The role of Intensivist is essential not only in the management of acute phases in chronic diseases, but also in the longterm management of a homely care.     

Pulmonary edema associated with the Chinese medicine shosaikoto

A 45-year-old Japanese woman presented with a high fever, a nonproductive coughing, and severe dyspnea, and was admitted to another hospital. During the week prior to hospitalization, she had been given Shosaikoto for treatment of liver dysfunction of unknown etiology. Mycoplasma pneumonitis was initially suspected, so she was treated with antibiotics (clindamycin and minocycline) and received oxygen therapy. Pulmonary insufficiency worsened rapidly, and she was transferred to our hospital. On admission, a chest roentgenogram revealed bilateral alveolar infiltrates predominantly in the medial lung fields. Furosemide and high-dose methylprednisolone were immediately administered, but hypoxemia increased. When the PaO2 was 55.7 Torr while the patient breathed 100% oxygen, mechanical ventilation with positive end-expiratory pressure (PEEP) was started. Arterial blood-gas values improved dramatically, and the chest roentgenogram became clear. Our diagnosis of noncardiogenic pulmonary edema is based on the chest-roentgenographic findings, infiltration of inflammatory cells as seen in two lung-biopsy specimens and bronchoalveolar lavage fluid, the lack of findings of heart failure on physical examination and electrocardiography, and the good clinical response to PEEP. A positive lymphocyte stimulation test in response to Shosaikoto implicated this non-traditional herbal medicine as an etiologic factor in the non-cardiogenic pulmonary edema. Shosaikoto has been identified as the cause of interstitial pneumonia or eosinophilic pneumonia, but pulmonary edema associated with Shosaikoto has not been previously described. This case suggests that methylprednisolone treatment may be insufficient for Shosaikoto-induced pulmonary edema, and that mechanical ventilation with PEEP is very effective.     

Complete response in severe thrombotic microangiopathy post bone marrow transplantation (BMT-TM) after multiple plasmaphereses

A 44-year-old male with Ph+ chronic myeloid leukaemia (CML) underwent histoidentical allogeneic bone marrow transplantation 18 months after initial diagnosis. He received pretransplant conditioning with busulphan and cyclophosphamide (Bucy). GVHD prophylaxis consisted of methotrexate, cyclosporine (CsA) and methylprednisolone. On day +50, he developed a microangiopathic haemolytic anaemia with indirect bilirubinaemia, 10% fragmented red cells (FC) and an elevated LDH (1213 U/l: normal range 100-185 U/l). Clinical symptoms consisted of edema and hypertension. The patient was not febrile and had no neurological changes. A clinical diagnosis of severe (grade 4) multifactorial (acute GVHD, CMV infection and cyclosporine) BMT-TM was made. He responded following 19 plasma exchanges with replacement with fresh frozen plasma.     

A case of spontaneous hemopneumothorax occurred after thoracic drainage

A 21-year-old man; complaining of left chest pain and dyspnea, was admitted to our hospital with a diagnosis of spontaneous pneumothorax. Though chest X-ray on admission did not show hemothorax, chest drainage revealed intrapleural bleeding. As chest X-ray on the following day showed evident fluid level, emergency operation was carried out with a diagnosis of spontaneous hemopneumothorax. Bleeding point was a ruptured vessel between parietal pleura and bulla in apex of lung. The bulla was resected following hemostasis. After improvement of complicating postoperative re-expansive pulmonary edema, the patient was discharged on the 18th postoperative day. On treatment of spontaneous hemopneumothorax, existence of such a case as ours should be taken into account.     

A case of severe cytomegalovirus infection after the repair of coarctation of aorta

We report a 2-month-old boy without any immuno-compromised diseases, who suffered from the severe cytomegalovirus (CMV) infection after the subclavian flap aortoplasty and pulmonary artery banding for coarctation complex. He underwent the operation at 2 months old and received 2 units of irradiated packed red blood cells before and after the surgery. His postoperative course was uneventful but the interstitial pneumonitis, until he developed watery diarrhea 10 days after the surgery following hepatitis with the marked hepatomegaly 3 weeks after. Since CMV infection was confirmed as the cause of the pneumonitis, enterocolitis and hepatitis, he was initially treated by gamma-globulin with the high CMV titer at a dose of 200 mg/kg/day for 2 days and ganciclovir at a dose of 10 mg/kg/day for 14 days. Because of the persistent CMV infection, he needed two more treatments of ganciclovir at the same dosage and gamma-globulin once a week for 2 months. He finally recovered from severe CMV infection 5 months after the above treatments. In conclusion, the severe CMV infection can occur by blood transfusion even in the surgical case with normal immune system. If one finds pneumonitis, hepatitis or enterocolitis after any type of surgery with history of blood transfusion, CMV infection should be suspected as the cause of these diseases.     

Venous leg ulcers. Part 1: Aetiology

Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who received mechanical ventilation at study entry comprised the intubation group. The rest of the patients were randomly assigned to either of the following 2 groups: 11 patients who received oxygen plus CPAP delivered by a nasal mask (CPAP group), and 11 patients who received oxygen only via face mask (oxygen group). All patients in the intubation group had cardiogenic shock. Two patients (18%) in the CPAP group and 8 patients (73%) in the oxygen group required mechanical ventilation with endotracheal intubation (p=0.03). The hospital mortality rate in the CPAP group (9%) was significantly lower than the oxygen group (64%, p=0.02). The pulmonary artery wedge pressure and heart rate were significantly lower in the CPAP group than in the oxygen group 24 h after study entry (p<0.05 and p<0.01). The mean pulmonary artery pressure 48 h after study entry was 18+/-5 mmHg in the CPAP group and 25+/-8 mmHg in the oxygen group (p<0.05). The PaO2/FiO2 ratio increased in the intubation group (168+/-69 to 240+/-57, p<0.05) and the CPAP group (137+/-17 to 253+/-67, p<0.01) 24 h after study entry. Arterial plasma endothelin-1 concentrations decreased significantly earlier in the CPAP group than in the oxygen group (p<0.05). In patients without cardiogenic shock, nasal CPAP lead to an early improvement in oxygenation and hemodynamics, and decreased the mortality rate. Early and active respiratory management is recommended in patients with pulmonary edema associated with acute myocardial infarction.     

Dilutional hyponatraemia: a cause of massive fatal intraoperative cerebral oedema in a child undergoing renal transplantation

A four year old boy with polyuric renal failure resulting from recurrent urinary tract infections and vesicoureteric reflux from birth underwent renal transplantation. In the past he had had five ureteric reimplant operations and a gastrostomy, as he ate nothing by mouth. He required peritoneal dialysis 13 hours a night, six nights a week. His fluid requirements were 2100 ml per day. This included a night feed of 1.5 litres Nutrizon. Before operation he received 900 ml of Dioralyte instead of the Nutrizon feed, and peritoneal dialysis was performed as usual. The operation itself was technically difficult and there was more blood loss than anticipated, requiring intravenous fluids and blood. The operation ended about four hours later but he did not wake up. Urgent computed tomography revealed gross cerebral oedema. He died the next day. At necropsy the brain was massively oedematous and weighed 1680 g.     

Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation

Mechanical ventilation with high peak inspiratory pressure and large tidal volume (VT) produces permeability pulmonary edema. Whether it is mean or peak inspiratory pressure (i.e., mean or end-inspiratory volume) that is the major determinant of ventilation-induced lung injury is unsettled. Rats were ventilated with increasing tidal volumes starting from different degrees of FRC that were set by increasing end-expiratory pressure during positive-pressure ventilation. Pulmonary edema was assessed by the measurement of extravascular lung water content. The importance of permeability alterations was evaluated by measurement of dry lung weight and determination of albumin distribution space. Pulmonary edema with permeability alterations occurred regardless of the value of positive end-expiratory pressure (PEEP), provided the increase in VT was large enough. Similarly, edema occurred even during normal VT ventilation provided the increase in PEEP was large enough. Furthermore, moderate increases in VT or PEEP that were innocuous when applied alone, produced edema when combined. The effect of PEEP was not the consequence of raised airway pressure but of the increase in FRC since similar observations were made in animals ventilated with negative inspiratory pressure. However, although permeability alterations were similar, edema was less marked in animals ventilated with PEEP than in those ventilated with zero end-expiratory pressure (ZEEP) with the same end-inspiratory pressure. This "beneficial" effect of PEEP was probably the consequence of hemodynamic alterations. Indeed, infusion of dopamine to correct the drop in systemic arterial pressure that occurred during PEEP ventilation resulted in a significant increase in pulmonary edema. In conclusion, rather than VT or FRC value, the end-inspiratory volume is probably the main determinant of ventilation-induced edema. Hemodynamic status plays an important role in modulating the amount of edema during lung overinflation but does not fundamentally modify the characteristics of this edema which is consistently associated with major permeability alterations. These results may be relevant for ventilatory strategies during acute respiratory failure.     

Accessory artificial circulation in complex treatment of experimental acute toxic pulmonary edema

In experiments on 50 dogs with toxic acute edema of the lung, induced with intravenous injection of 0.1% silver nitrate, the authors have studied the efficacy of accessory artificial circulation and "conservative" therapy. During the perfusion a discharge of the right portions, adequate extracorporeal gas metabolism, normalization of blood gas and acid-base balance were noted; an intensity of pulmonary edema is descreased. An intensive therapy for pulmonary edema was found to be more effective in association of "conservative" treatment with venoarterial perfusion and blood oxygenation.     

Role of nitric oxide in sepsis-associated pulmonary edema

Transient pulmonary hypertension after inhibition of nitric oxide synthase (NOS) does not alter pulmonary reflection coefficients or lymph flows in endotoxemic sheep. To test the effects of persistent pulmonary hypertension induced by N omega-nitro-L-arginine methylester (L-NAME) and of inhaled NO on pulmonary edema, 18 sheep (three groups) were chronically instrumented with pulmonary artery catheters, femoral arterial fiberoptic thermistor catheters, and tracheostomy. The awake, spontaneously breathing animals received Salmonella typhi endotoxin (lipopolysaccharide; LPS) (10 ng/kg/ min) for 28 h. After 24 h, an airflow of 6 L/min was delivered through the tracheostomy. One group of animals (L-NAME/air) received L-NAME intravenously (25 mg/kg + 5 mg/kg/h) and breathed air. The second group (L-NAME/NO) was given L-NAME and NO (40 ppm) was added to the airflow. The third group was given NaCl 0.9% and breathed air (NaCl/air). Extravascular lung water was measured through the double-indicator dilution technique. Endotoxemia caused pulmonary edema, which was aggravated by L-NAME. Breathing of NO normalized pulmonary artery pressure (Ppa) and ameliorated pulmonary edema. Inhalation of NO may therefore be a therapeutic option for pulmonary edema associated with pulmonary hypertension.     

An autopsy case of severe tuberculosis associated with anal fistula and intestinal perforation

A 55 year-old man was admitted to the department of the gastroenterology of the hospital because of severe weakness and appetite loss for the past one month. In the last two months, he has been suffering from recurrent fistula of the anus. He left his symptoms without therapy. A gastric ulcer was found out with gastric endoscopy. At the same time, chest X-ray film showed bilateral abnormal shadows, which were suspected of severe pulmonary tuberculosis by a chest physician. After the admission, the patient immediately developed respiratory failure. Both sputa and discharge from anal fistula were positive for acid fast bacillus. Despite of anti-tuberculosis therapy and mechanical ventilation, he died of respiratory failure. At the autopsy, severe pulmonary tuberculosis, tuberculous fistula of the anus, intestinal tuberculosis with perforation, miliary tuberculosis and peptic ulcer of the stomach were defined. We suspected that the extensive disease caused by hematogeneous spread and the late diagnosis of tuberculosis was owing to patient's delay.     

Pulmonary edema in obstetric patients is rapidly resolved except in the presence of infection or of nitroglycerin tocolysis after open fetal surgery

OBJECTIVES: This study was designed to determine the etiology, course, and severity of pulmonary edema in obstetric patients in a tertiary care center. STUDY DESIGN: A retrospective study was carried out on 16,810 deliveries from University of California, San Francisco, 1985-1995. Diagnosis and severity of lung injury were defined by a 4-point system that was based on the chest radiograph, oxygenation, positive end-expiratory pressure, and lung compliance. Resolution of pulmonary edema was defined by improvement in the chest radiograph and hypoxemia (ratio of arterial oxygen tension to inspired oxygen concentration) scores or by extubation. RESULTS: Pulmonary edema developed in 86 patients, or 0.5% of all obstetric cases. It usually showed extensive air space consolidation on the chest radiograph and arterial hypoxemia. Although 43% of the patients had severe pulmonary dysfunction, the average time to resolution of pulmonary edema was 2.4 days. Only 45% of patients required admission to the intensive care unit and only 15% required intubation and positive-pressure ventilation. Patients with infection (mean of 7.2 days) or fetal surgery (mean of 3.8 days) had the most severe, protracted course. CONCLUSION: Although obstetric pulmonary edema is associated with extensive radiographic infiltrates and severe hypoxemia, resolution occurs rapidly in most patients, limiting the need for intensive care support.     

The diameter of callus in leg lengthening: 28 tibial lengthenings in 14 patients with achondroplasia

A 46-year-old man who had been pulled under water by a tidal wave when an earthquake occurred on July 12, 1993 was carried to our hospital the next day. He soon needed endotracheal intubation and mechanical ventilation because he expectorated sputa with sand and because arterial bloodgas analysis revealed severe hypoxemia. Chest X-ray on admission showed diffuse small nodules and areas of consolidation. Chest CT obtained on July 16 showed centrilobular small nodules bilaterally and alveolar opacities in the peribronchial region. After therapy with antibiotics and frequent bronchial lavages, sputum with sand disappeared on the 14 th hospital day and chest X-ray film and laboratory data showed marked improvement. He was discharged on October 1. A chest CT scan obtained on February 17, 1994 showed improvement of the small nodules. The areas of consolidation had also improved, but remained as linear and nodular opacities, which were considered to be organized lesions. There are few reports concerning radiographic findings particularly CT findings, after aspiration of sea water and sand during near drowning.     

Characterization of a new HLA-B39 allele, B*3913, in a Brazilian Caucasian

We report a case of paraplegia in the immediate postoperative period following right bilobectomy for carcinoma of the lung. An epidural catheter had been inserted following induction of anaesthesia and an infusion of bupivacaine 0.15% was used for postoperative pain relief. Magnetic resonance imaging failed to reveal any spinal or epidural haematoma or spinal cord ischaemia. The patient developed respiratory failure on the third postoperative day and required assisted ventilation. He was weaned from the ventilator on day 15. Two days later he sustained a cardiac arrest and died. Post-mortem examination demonstrated spinal cord infarction and severely stenosed spinal arteries. The thoracotomy position and/or intra-operative hypotension might have compromised the blood flow to the spinal cord and although suspected as a possible cause, the use of epidural analgesia was not implicated.     

Birth in triplet pregnancies. Vaginal delivery--how often is it possible?

The patient was born by emergency cesarean section for fetal distress at 35 weeks gestation with a weight of 2740 g. The early neonatal course was complicated by transient tachypnea and renal failure. He was receiving oxygen and diureticus in incubator for 5 days and his condition was very improved on day 5. On day 7 he became lethargy and there was inability to tolerate feeding. Investigation of the cerebrospinal fluid revealed 8,000 leukocytes/microliter. S. marcescens was grown from cultures of both blood and cerebrospinal fluid. Treatment was started with cefotaxime and ampicillin every 6 hour. On day 14 the CT showed a brain abscess located parietooccipitally on the left side and diffuse infarction on the right side. On day 14 and 23 recurrence of increased leukocytes in the cerebrospinal fluid, high values of serum CRP and deterioration of clinical symptoms were observed. It is thought that the episodes show rupture of the abscess into the lateral ventricle. On day 55 surgical drainage was performed for the hydrocephalus. On day 110 the abscess was not found in the brain CT scan. His psychomotor development 3 years later was equivalent to two years old and he had secondary epilepsy.     

Effective immunoglobulin therapy for brief tonic seizures in methylmalonic acidemia

We report on a patient with methylmalonic acidemia (MMA). He experienced a metabolic acidosis attack at 3 weeks of age. He immediately received peritoneal dialysis and exchange transfusion, and recovered from the attack. His MMA phenotype was mut0. Dietary therapy (strict protein restriction) was found to be effective in preventing further attacks, and he had mild hypotonia and impaired psychomotor development. At 9 months of age, he developed brief tonic seizures, which showed polyspike bursts under EEG. His psychomotor development continued to deteriorate. However, intravenous administration of immunoglobulin (200 mg/kg/day for 5 consecutive days) had a dramatic effect; his seizures disappeared and his psychomotor development improved.     

Combined chemotherapy with low-dose cisplatin, tegafur and uracil in a case with neck recurrence of laryngeal cancer

The patient was a 60-year-old man with progressive neck recurrence of laryngeal squamous cell carcinoma. As a previous treatment, he had undergone irradiation (primary: 60 Gy; neck: 45 Gy) after two cycles of neoadjuvant chemotherapy (cisplatin 100 mg/m2 daily; day 1:5-fluorouracil 1,000 mg/m2 daily; day 1-5) and planned neck dissection. For a neck recurrence, he had received five cycles of low-dose cisplatin (5 mg/body daily: day 1-5) with tegafur and uracil (600 mg/body daily: day 1-7) every week. As an outpatient, he then received ten cycles of low-dose cisplatin (10 mg/body daily: day 3, 6) with tegafur and uracil (600 mg/body daily: day 1-7) every week. The size of the tumor did not decrease with the above chemotherapy, but no remarkable growth of the cancer was seen, and no toxic effect of the chemotherapy was observed. He continued his job for 30 weeks just as before he had fallen sick. Chemotherapy of low-dose cisplatin with tegafur and uracil was suggested to be useful for the patient with recurrent laryngeal squamous cell carcinoma.     

Effect of pulmonary microembolism on arteriovenous shunt flow

The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.