Cases reported "Anoxia"

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1/34. Transient swallow syncope during periods of hypoxia in a 67-year-old patient after self-extubation.

    OBJECTIVE: To describe the case of an adult patient with swallow syncope after bypass surgery, possibly related to hypoxia. DESIGN: Case report. SETTING: University hospital, medical-cardiologic intensive care unit. PATIENT: A 67-yr-old patient after second aortocoronary bypass operation for unstable angina. MAIN RESULTS: After the patient managed to extubate himself, he was in a borderline respiratory condition with an oxygen mask. When drinking for the first time after extubation, asystole was observed coincidentally with interruption of oxygen insufflation. During the next days, similar events occurred during food ingestion or when drinking liquids after a fall of oxygen saturation. The bradyarrhythmia was readily reversible on administration of atropine and ventricular backup pacing via temporary pacing wires. After normalization of gas exchange, no more episodes of swallowing-associated asystole were observed and the patient was discharged without a permanent pacemaker. There was no esophageal or gastrointestinal disease. Pre- and postoperative PR and QRS durations were normal. CONCLUSION: Extrinsic and transient mechanisms, rather than intrinsic conduction system disease, seem to have been operative in this case. It is suggested that hypoxia reinforced the vagal pharyngocardiac reflex as described in pediatric patients.
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2/34. Low-dose inhaled nitric oxide in term and near-term infants with hypoxic respiratory failure: a Malaysian experience.

    Inhaled nitric oxide (iNO) improves oxygenation in term and near-term infants with persistent pulmonary hypertension of the newborn (PPHN) and decreases the need for treatment with extracorporeal membrane oxygenation (ECMO). This mode of treatment is currently being introduced in malaysia. We report our preliminary experience using low dose inhaled nitric oxide (20 parts per million) in three newborn infants (meconium aspiration syndrome, primary PPHN and congenital diaphragmatic hernia) with severe PPHN who fulfilled criteria for ECMO with a mean oxygenation index (OI) of 40. Two of the infants showed rapid and sustained improvement in oxygenation with a reduction in oxygenation index (OI) over 24 hours. The infant with diaphragmatic hernia showed an initial improvement in OI, which was unsustained and subsequently died. All three infants did not show significant elevation of methemoglobin or nitrogen dioxide (NO2). Inhaled nitric oxide is an effective and safe treatment for severe PPHN that can be used in a developing country like malaysia.
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3/34. Acute right-to-left inter-atrial shunt; an important cause of profound hypoxia.

    Three patients presented to our intensive care unit over a 3-yr period with profound hypoxia resulting from acute right-to-left inter-atrial shunt (RLIAS). Patient 1 was a 67-yr-old male with an atrial septal defect who became hypoxic and developed the rare sign of platypnoea following elective repair of an abdominal aortic aneurysm (breathlessness made worse when upright and relieved by lying flat). Patient 2 was a 38-yr-old female who developed platypnoea and hypoxia secondary to a patent foramen ovale (PFO) and pericardial effusion. Patient 3 was a 46-yr-old male with a PFO who developed hypoxia without platypnoea because of multiple pulmonary emboli following right hemicolectomy. These case reports illustrate the need to consider RLIAS as a cause of hypoxia of sudden onset. Early use of bubble contrast echocardiography is indicated.
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4/34. Mitral atresia with premature closure of foramen ovale. A rare hemodynamic cause for failure of Blalock-Taussig anastomosis to relieve inadequate pulmonary blood flow.

    The clinical, hemodynamic, and surgical findings encountered in the management of a hypoxic male infant with a rare and complex variety of cyanotic congenital heart disease associated with inadequate pulmonary blood flow are described. A poor clinical response to creation of a Blalock-Taussig anastomosis led to the discovery of mitral atresia complicated by premature closure of the foramen ovale and partially relieved by the presence of a levoatriocardinal vein. The subsequent creation of an atrial septal defect enhanced the function of the subclavian artery to pulmonary artery anastomosis and provided palliative relief of hypoxia. Some of the clinical and laboratory findings indicating the presence of additional lesions complicating the picture of a tetralogy of fallot and requiring additional surgical considerations are discussed. The experience indicates that hemodynamic as well as surgical causes may explain the failure of a systemic artery to pulmonary artery anastomosis to function adequately and should be sought.
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5/34. Unusual facial markings and lethal mechanisms in a series of gasoline inhalation deaths.

    A review of deaths associated with hydrocarbon toxicity from gasoline sniffing in south australia throughout a 10 year period from July 1987 to June 2002 revealed 4 cases. The victims were all Aboriginal people from remote inland communities. Each death had occurred while the victim was lying in bed sniffing gasoline from a can held to the face. Once unconsciousness had occurred, the mouth and nose had been pressed firmly against the can by the weight of the head. In each case, the effects of gasoline toxicity had been exacerbated by hypoxia and hypercapnia from rebreathing into the container once a tight seal had been established between the face and the can. The circular impressions left by the can edges on the faces of each of the victims provided an autopsy marker that assisted in clarifying the details of the fatal episodes. Discouraging solitary gasoline sniffing in bed may reduce the death rate in communities where this behavior is practiced.
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6/34. granulocyte colony-stimulating factor-induced capillary leak syndrome confirmed by extravascular lung water measurements.

    The study purpose was to report the first case of granulocyte colony-stimulating factor (G-CSF)-induced capillary leak syndrome (CLS) in which serial extravascular lung water (EVLW) measurements were performed and to compare this case with previously reported cases. To identify previously reported cases, we performed a literature search, using pubmed with the following search terms: CLS, EVLW, G-CSF, granulocyte-macrophage colony-stimulating factor (GM-CSF) and stem cell transplantation and the references in the bibliographies of the papers retrieved. To obtain additional information about these cases, we contacted the authors by e-mail. We describe the case of a 68-year-old woman who developed severe CLS during G-CSF treatment after autologous haematological stem cell transplantation. CLS is caused by damage to the endothelial cells, resulting in extravasation of plasma proteins and fluid from the capillaries into the extravascular space. This is illustrated by high values of EVLW and pulmonary vascular permeability, necessitating mechanical ventilation. We found five other case reports in the literature. The white blood cell count at the onset of the CLS varied from very low (zero) to very high (90,500/mul). The symptoms began on day 5-9 of the G-CSF treatment. All patients had fever. Three patients were mechanically ventilated and four received renal replacement therapy. Two patients died. Treatment with G-CSF can induce fatal CLS. Monitoring of EVLW in patients with severe CLS may be useful to guide fluid therapy and improve oxygenation.
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7/34. Posthypoxic myoclonus (the Lance-Adams syndrome) in the intensive care unit.

    The neurological assessment of patients admitted to the intensive care unit after successful resuscitation from cardiopulmonary arrest may be difficult. We describe the cases of two patients who developed myoclonus within 24 hours of hypoxic respiratory and cardiac arrest. Initially, the clonic movements were thought to be generalised convulsions and were treated as such, until it became evident that the patients were aware and distressed. Posthypoxic myoclonus is a rare complication of successful cardiopulmonary resusitation. Recognition depends on the awareness that the syndrome exists, and is important so that correct therapy can be instituted. There may be important prognostic implications. Both our patients had normal intellectual recovery with moderate residual neurological disability from their movement disorder.
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8/34. Acardius anceps: report of 3 cases.

    Acardius anceps is an uncommon but serious consequence of multiple pregnancy, usually in monozygotic twins. There are great variations in gross appearance and pathologic features. Recently we have encountered 3 cases of acardius anceps in 3 sets of twin pregnancy. The subcutaneous edema was so extensive and severe that no facial structures could be recognized; however, the skull bones could be detected by prenatal ultrasound examination and confirmed by postnatal radiography. The hearts were all severely malformed and many of the visceral organs were also defective. Prenatal blood gas analysis in 2 affected fetuses showed severe hypoxemia. All 3 pregnancies were terminated before the normal co-twin reached viability. One set of the twins was delivered by hysterotomy because of the potential dystocia caused by bulky fetal mass due to severe hydropic change. Prenatal ultrasound examination is a very useful tool in the diagnosis and management of this anomaly.
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9/34. Pathological findings in a case of hypoxic myoclonus treated with 5-hydroxytryptophan and a decarboxylase inhibitor.

    A 72-year-old woman suffered a respiratory arrest following intoxication with barbiturates. Her examination 27 months after the anoxic incident revealed involuntary jerks of trunk and limb muscles triggered by willed movements. On a regimen of 1 g L-5-HTP and 100 mg l-alpha-methyldopa hydrazine (carbidopa), action myoclonus disappeared completely. This medication had to be discontinued because of a regressive hysterical reaction. Two months later, she was found unconscious; resuscitation efforts were unsuccessful. autopsy showed death was caused by choking on food. Coronal slices of the cerebral hemispheres and transverse section of the brainstem and cerebellum revealed no lesion. No evidence of hypoxic damage could be demonstrated in the cerebral cortex, hippocampus, striatum, pallidum, subthalamus, thalamus, or other diencephalic structures. In the caudal half of the midbrain tegmentum, a marked astrocytic reaction of some duration was encountered in the lateral parts of the supratrochlearis nucleus, the lateral subnucleus of the mesencephalic gray, and the immediately adjacent cuneiform and subcuneiform nuclei. In the former nucleus, sites of presumed nerve cell disintegration were found, but the neuronal populations of this nucleus and of the other raphe nuclei were well maintained. The other brainstem structures and the cerebellum were normal. Our neuropathological findings suggest that hypoxic myoclonus (a) does not seem to be explained by demonstrable neuronal loss in motor structures, such as cerebellum, thalamus, or basal ganglia and (b) does not appear to be causally related to a detectable reduction in the serotonin-containing neurons of the brain but rather to a functional derangement of anatomically intact serotonergic pathways originating perhaps from other, as yet unidentified, damaged neuronal structures.
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10/34. dialysis leukopenia and hypoxemia in a patient without measurable complement activity.

    We have studied complement activity, total leukocyte counts, PO2 and acid-base balance during a single hemodialysis with cuprophan membranes in a patient with hereditary angioedema and C3NeF-positive chronic membranoproliferative glomerulonephritis. Before, during and after the dialytic procedure plasma complement activity (total hemolytic complement, classical and alternative pathway activities) was not detectable and no C3-conversion occurred, while profound leukopenia (from 8,500 to 1,800 leukocytes/microliter) and hypoxemia (from 101.8 to 86 mmHg PO2) were found within 20 min from the initiation of hemodialysis. Similar results were obtained by studying the same parameters during two additional hemodialytic procedures. in vitro experiments showed that the patient's C3 could not be converted, either by cuprophan or zymosan, a specific and potent complement activator, even under optimal experimental conditions. Our data demonstrate that complement activation is not the only possible mechanism responsible for early leukopenia (as well as hypoxemia) during dialysis with cuprophan membranes.
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