Intense Cyanosis Research Articles

Complete Abnormal Venous Return Associated with Complex Heart Disease: Case Report S. Faiz, M. Boussif, B. Zouita, D. Basraoui, H. Jalal Published: April 27, 2024 | 4 2 DOI: 10.36347/sjmcr.2024.v12i04.035 Pages: 531-533 Downloads Abstract Total anomalous pulmonary venous return (TAPVR) is a cardiac malformation defined by a complete absence of communication between the pulmonary veins and the left atrium. All

Total anomalous pulmonary venous return (TAPVR) is a cardiac malformation defined by a complete absence of communication between the pulmonary veins and the left atrium. All oxygenated pulmonary venous return flows directly or indirectly into the right atrium. Survival is only possible via a right-to-left atrial shunt. Non-blocked forms present as high-flow shunts with moderate cyanosis. Symptoms in blocked forms are dominated by obstruction of venous return, and life-threatening distress with intense cyanosis and severe pulmonary hypertension sets in from the very first days of life. Treatment consists in connecting the pulmonary venous receptacle to the left atrium, tying off the collector and closing the inter-atrial septum. The risks of surgery remain high in severe forms, and failures usually occur in the first year of life. In the case of good surgical correction, the long-term prognosis is excellent.

REVIEW ON CYANIDE POISONING

Cyanide is one of the most lethal poison. It leads to death within a few minutes to a few hours sometimes. Depending upon the dose and route of administration or exposure the symptoms develop. The area of exposure is manufacturing and industrial sources such as insecticides, photographic solution, fumigation and electroplating work, plastic manufacturing and jewelry cleaners etc. History shows the common use of cyanide poisoning in suicidal and homicidal cases and also use as chemical warfare agent for terrorist attack. Incidence of cyanide poisoning is rare but the occurrence of death is seen instant in some cases. It causes histotoxic anoxia and inhibits oxidative phosphorylation, a process where oxygen is utilized for the production of essential cellular energy sources in the form of ATP. It does so by binds to the enzyme cytochrome C oxidase and blocks mitochondrial transport chain. This results in cellular hypoxia and the depletion of ATP occur, leading to metabolic acidosis. Symptoms such as headache, dizziness, vertigo, spasmodic closure of jaw and clawing of hands, tonic type of convulsions of the limb and trunk, muscular weakness and flaccidity, muscular paralysis, intense cyanosis, hypertension followed by hypotension, coma etc leads to death. Death is mainly due to cardiovascular failure and respiratory failure. Thus, rapid treatment to be started in such patients. The 100 % oxygen support and rapid therapy of antidotal treatment is necessary for life saving. Very efficient antidote is Hydroxocobalamin and other antidotes are also important in cyanide poisoning in the treatment as life saver. Survivors of cyanide poisoning may develop neuropathies.

Inhalation of helium in plastic bag suffocation with suicidal purpose: Observation and differences of two cases.

The use of helium in plastic bag suffocation is a suicide method recently found in forensic cases. Although it is not common practice, there has been a strong increase in its use during the past 20 years, thanks to the accessibility of information on the web and materials needed to implement it. From a pathophysiological point of view, there are various theories on how helium can change the timing and, also, the cause of death when the head is inside a plastic bag. We report two cases where we believe that the action of helium, whose unequivocal use is demonstrated by the circumstantial data, has unfolded in a different way. In the first case, the discovery of an intense cyanosis of the face, blood leakage from the respiratory orifices and the destruction of numerous alveolar septa with histologically demonstrated blood extravasation, was left for a longer agonic period and a no negligible rate of pulmonary barotrauma in determination of death. In the second case, the total absence of external pathological phenomena, internal and histological, allows us to hypothesise an onset of death that is faster and catalysed by helium and explained by the known sympathetic hyperactivation and consequent cardiac arrhythmic death described in similar plastic bag suffocation cases.

Serratia Marcescens Sepsis in a Child with Deep Venous Thrombosis - A Case Report.

Venous thromboembolism is a rare condition in paediatrics that included both deep venous thrombosis and pulmonary embolism. Serratia marcescens is a gram-negative bacterium that belongs to the Enterobacteriaceae family and tends to affect immunocompromised hosts. We report the case of an 11-year-old boy, admitted in the Pediatric Clinic I from Emergency County Hospital Tîrgu Mureş, Romania with intense pain, swelling, cyanosis and claudication of the left foot. His personal history revealed a recent appendectomy. A close family was reported to have had a deep venous thrombosis. The laboratory tests, performed on the day of admission, revealed increased inflammatory biomarkers and D-dimer. Coagulation tests gave a low activated partial thromboplastin time (APTT). Doppler venous ultrasound and CT-exam established a diagnosis of deep venous thrombosis. Anticoagulant therapy was initiated, but on the tenth day of admission, the patient developed signs and symptoms of sepsis, and the blood culture revealed Serratia marcescens. After antibiotic and anticoagulant therapy, the patient progressed favourably. The patient was a carrier of the heterozygous form of Factor V Leiden. The association between deep venous thrombosis and Serratia marcescens sepsis can compromise a condition in pediatric patients.

A Difficult Emergency Surgical Diagnosis: Atresia of the Common Pulmonary Vein

A newborn female experienced severe respiratory distress immediately after delivery. She presented with intense cyanosis, refractory hypoxemia, and acidosis. The deterioration was rapidly progressive, leading to the child's demise. The autopsy showed common pulmonary vein atresia, the most severe form of pulmonary venous drainage obstruction. Subpleural and interstitial pulmonary lymphagiectasias also were present as well as evidence of pulmonary hypertension. The lung pathology probably resulted from pulmonary venous atresia during prenatal development.

Iatrogenic tension pneumothorax in children: two case reports

IntroductionTwo cases of iatrogenic tension pneumothorax in children are reported.Case presentationsCase 1: A 2-year-old boy with suspected brain death after suffering multiple trauma suddenly developed intense cyanosis, extreme bradycardia and generalized subcutaneous emphysema during apnea testing. He received advanced cardiopulmonary resuscitation and urgent bilateral needle thoracostomy. Case 2: A diagnostic-therapeutic flexible bronchoscopy was conducted on a 17-month-old girl, under sedation-analgesia with midazolam and ketamine. She very suddenly developed bradycardia, generalized cyanosis and cervical, thoracic and abdominal subcutaneous emphysema. Urgent needle decompression of both hemithoraces was performed.ConclusionIn techniques where gas is introduced into a child's airway, it is vital to ensure its way out to avoid iatrogenic tension pneumothorax. Moreover, the equipment to perform an urgent needle thoracostomy should be readily available.

Presentation of Congenital Heart Disease in the Neonate and Young Infant

Presentation of Congenital Heart Disease in the Neonate and Young Infant

Respiratory Complications Due to Nitrous Oxide Impurities Six cases

The impurities potentially contained in nitrous oxide cylinders include NO, , CO and . The consequences of inahaling NO and are reflex breathing inhibition with laryngospasm and the rapid onset of intense cyanosis due to altered pulmonary gas exchange and methaemoglobinemia. Pulmonary edema may occur in the acute stage. Chronic chemical pneumonitis may follow with resultant pulmonary fibrosis and the respiratory and metabolic acidosis may also occur. Hypotension may be marked and results from the effects of nitrate and nitrite ions on vascular smooth muscle. Since certain clinical features provide clues that allow practicing anesthetists to recognize the toxicities of higher nitrogen oxides, six of our cases will be described in detail, whereas the remaining cases will be only commented. We examined a cylinder at the National Metrology Institute, its concentration was 2359 ppm. Another two cylinders were also abnormal with concentrations of 547 ppm and 180 ppm. We recommend that medical gases be subjected to quality control on a national basis.

The Effect of Intense Passive Apnea in the Acid-Base Balance and Electrolytes

The aim of this study was to investigate the disturbances of the acid-base balance and electrolyte disorders in healthy individuals in the greatest passive apnea (prior to apnea and prior to first inhalation). The changes of the acid-base balance, the serum potassium and calcium levels as well as the disturbances of the cardiac rhythm were studied in a group of 15 healthy males aged 18 to 41 years old. Seven individuals part of the original group participated in a second trial. Following the initial apnea trial the individuals were allowed to 2–3 free inhalations and a second passive apnea effort was performed. The same parameters were measured in the second effort. In the primary effort the apnea duration was 170 ± 53 s (mean ± SD). The results received prior to the effort and immediately before the end of the apnea (paired t-test), showed no significant changes in the blood pH. The PaCO2 increased significantly, the PaO2 decreased significantly, blood bicarbonate increased significantly, the hemoglobin oxygen saturation decreased significantly. In addition the serum potassium and calcium levels decreased significantly. In the subgroup (7 individuals) the second effort of apnea lasted 50–70 s and showed no significant changes in the blood pH. The same changes concerning PaCO2 and blood bicarbonate were observed in the first and second effort of passive apnea. The serum potassium and calcium levels as well as the hemoglobin oxygen saturation showed no significant changes. During the initial effort of apnea all men presented bradycardia, which was followed by tachycardia immediately after the end of the effort. One individual, whose effort lasted 290 s suffered intense tachycardia, cyanosis, convulsions, and loss of consciousness. It is concluded that during an intense effort of passive apnea: (a) the blood PaCO2 is significantly increased, as well as the blood bicarbonates, (b) the PaO2, the hemoglobin oxygen saturation and the serum potassium and calcium levels are significantly decreased, (c) the cardiac rate is significantly decreased, and (d) the second effort of apnea, following immediately the initial one, is sorter in duration and produces similar or milder changes of the above parameters.

Persistent pulmonary arterial hypertension of the newborn.

Persistent pulmonary hypertension of the newborn (PPHN) characterised by right to left shunting with intense cyanosis is difficult to manage, and in the best of centres carries a 40-60 percent mortality. We report our one year's experience of managing six neonates with PPHN. There were 5 males and 1 female with mean birth weight of 2.59 +/- 0.487 kg and gestation period 39 +/- 2.0 wks and 1 minute Apgar score 2.8 +/- 2.1. Four to six babies were born by cesarean section and 3-6 babies had aspiration pneumonia. All babies presented within 12 hours of age (mean 5.08 +/- 5 hrs) with intense cyanosis and respiratory distress. Diagnosis were confirmed in all by (a) hyperoxia test, (b) simultaneous determination of preductal and postductal paO2 (c) contrast echocardiography and (d) hyperoxia-hyperventilation test. Babies were managed with hyperventilation using mean ventilatory rates of 100 +/- 45 per minute, an inspired oxygen concentration of 100%, peak inspiratory pressures 27 +/- 9 cm of H2O, and expiratory pressures 5 +/- 1.6 cms of H2O, and mean air way pressures of 10.4 +/- 2.7 cms H2O. Alkali therapy was used in 3 of the six babies whereas low dose dopamine was infused in all six babies. Inspite of aggressive ventilatory therapy, only 3 out of 6 babies could be salvaged.

Delayed Sulfhemoglobinemia after Acute Dapsone Intoxication

A case of acute Dapsone intoxication due to voluntary ingestion of 3 g of this drug as a suicide attempt is described. A severe methemoglobinemia developed, accompanied by intense cyanosis, dyspnea, headache, and nausea. Subsequently, significant sulfhemoglobinemia responsible for prolonged cyanosis was observed, as well as mild hemolytic anemia. Relapses of methemoglobinemia after methylene blue treatment required repeated administration of the reducing agent. The need of a careful follow-up for several days in this type of intoxication is emphasized.

Methemoglobinemia from overdose of phenazopyridine hydrochloride

A case of severe methemoglobinemia and hemolytic anemia following ingestion of 5.6 gm of phenazopyridine with suicidal intent by a 16-year-old woman was successfully treated with intravenous methylene blue. Methemoglobinemia was suspected in this patient because of her intense central cyanosis, chocolate-colored blood, and minimal dyspnea. The patient's peripheral blood smear exhibited "bite cells." To the best of our knowledge, this is only the third such case reported in the literature. The pathophysiology, diagnosis, and therapy are reviewed.

Benzocaine-induced methemoglobinemia

Intense cyanosis in a previously well, 30-month-old, white girl was found to be due to the ingestion of benzocaine. A wide variety of chemical compounds present in many proprietary products, when ingested, can cause this presentation in individuals with structurally normal hemoglobin and normal activity of methemoglobin reductase. The phenomenon appears to be dose-related. Immediate recognition and initiation of appropriate therapy will effect a rapid reversal of the methemoglobinemia, and in some cases, may be life-saving. Caution should be exercised in the use of benzocaine-containing preparations.

THE TRIAD OF CYANOSIS, DECREASED PULMONARY VASCULARITY AND CARDIOMEGALY: Clinical, Pathologic, and Physiologic Considerations

The clinical findings in patients with the triad of cyanosis, cardiomegaly, and decreased pulmonary vascular markings are discussed as they relate to severe Ebstein's anomaly of the tricuspid valve, severe pulmonic valve stenosis, and pulmonic valve atresia with an intact ventricular septum. These entities may have certain pathologic anatomic features in common, including a right ventricle with a smaller functional capacity than normal, malformations of the tricuspid valve, hypoplasia of the pulmonary vascular bed, an enlarged right atrium, and right ventricular outflow tract obstruction. Similarly, these disorders often have a common pathophysiology, which includes impedance to right heart flow causing decreased pulmonary flow, a right-to-left shunt at the atrial level with peripheral arterial desaturation, tricuspid valve regurgitation, and right atrial hypertension. Since the infants under discussion often are gravely ill, decisions regarding their care may have to be made on the basis of clinical information alone without performing the definitive laboratory procedure, right ventricular selective angiocardiography. The clinical features that should alert the radiologist to the diagnosis of Ebstein's anomaly are that the defect is compatible with life to middle age, cyanosis in the neonatal period improving or disappearing with time, and an electrocardiogram showing arrhythmias, Wolff-Parkinson-White syndrome or right bundle branch block, prolonged PR and QRS intervals, and neither left nor right ventricular hypertrophy. Severe pulmonary valve stenosis is suggested when clinical information includes distress early in life in a cyanotic child with superior physical development and a harsh systolic murmur. The electrocardiogram typically shows severe right ventricular hypertrophy and “strain,” particularly as the child gets older. Pulmonic valve atresia should be suspected when a cyanotic child has congestive heart failure within the first few days or weeks of life, with intense cyanosis. The second sound is single, and the electrocardiogram may show left ventricular or right ventricular hypertrophy. With the plain film findings, this clinical information should permit a logical diagnosis, often before selective right ventricular angiocardiography.

An Unusual Case of Cyanotic Heart Disease: Atrial Septal Defect with Acquired Tricuspid Insufficiency

A rare case of tricuspid insufficiency due to bacterial endocarditis in association with a previously asymptomatic atrial septal defect is presented. Intense cyanosis, polycythemia and clubbing of digits were the major presenting clinical features. The classic physical findings of tricuspid insufficiency were not present. Hemodynamic data, blood gas analysis, and cine-angio-graphic studies are included. Surgical correction of the cardiac defects was successful.

Traumatic rupture of the chordae tendineae of the tricuspid valve: Successful repair twenty-four years later

A unique case of traumatic rupture of the chordae tendineae of the tricuspid valve with associated intense cyanosis and successful repair 24 years later has been reported. The clinical findings, hemodynamic and angiographic data, details of the surgical correction, and a year and a half follow-up of the patient have been included.

An Experimental Obliterating Thromboangiitis Limited to the Posterior Part of the Body*

After a brief outline of the principles involved in the production of thrombohemorrhagic phenomena (THP) with special organotropic localizations, an experimental technique is described which permits the production of acrocyanosis and thrombohemorrhagic lesions largely limited to the posterior part of the body. This phenomenon can be consistently produced by certain combinations of THP elicitors, anaphylactoid agents and noradrenaline (NA). The most effective combination among those tested is thorium dextrin (Th-Din) plus tannic acid plus NA. Several drugs can decisively influence the course of this reaction. Most otable among these are Neo-Antergan (an antihistaminic) which sensitizes for the production of the aboral THP, while heparin (presumably through its anticoagulant effect) and Dibenamine (presumably through its antiadrenergic action) offer virtually complete protection. When only Th-Din plus tannic acid is given, there develops an intense but reversible cyanosis in the hind paws and tail; additional treatment with NA induces obliterating thromboangiitis with hemorrhages and gangrene. None of hese changes are produced by Th-Din, tannic acid or NA alone. Evidently, here, e are dealing with pluricausal experimental diseases whose possible relationship to Raynaud's disease, thromboangiitis obliterans and anaphylactoid purpura is briefly discussed.

Pulmonary atresia and stenosis with intact ventricular septum.

Severe pulmonary stenosis or atresia with intact ventricular septum falls within the group of cardiac malformations which are characterized functionally by obstruction to pulmonary flow at the right side of the heart. This malformation is commonly manifested clinically by intense cyanosis, cardiac failure, and death in the neonatal period. Whereas the diagnosis and management of pulmonary stenosis in older children and adults is well established, there are relatively few published data relating to atresia or severe stenosis in infants having neonatal difficulties. In 1951, Johnson and Johnson 1 reported 5 patients with pulmonary stenosis who died between 3 and 19 months of age. Subsequently, others 2-4 having similar experiences have stressed the importance of early diagnosis and surgical correction. Pulmonary atresia (complete fusion of valve cusps) and severe pulmonary stenosis (extremely tiny or pinpoint orifice) may present similar or identical pictures. Cases with pulmonary atresia or severe stenosis may be

Arterial oxygen unsaturation and the ventilation-perfusion defect of Laennec's cirrhosis.

THE association of Laennec's cirrhosis with arterial oxygen unsaturation has been recognized but not satisfactorily explained. We have previously reported observations on a patient with Laennec's cirrhosis who had intense cyanosis, clubbed fingers and marked arterial oxygen unsaturation.1 The present study was designed to determine the incidence and the pathophysiologic basis of this phenomenon in patients with cirrhosis. Material and Methods Fifty-seven patients were studied. Fifty-six had far advanced Laennec cirrhosis associated in most cases with a background of excessive alcoholic intake. In the patients in whom the clinical and laboratory findings were equivocal, the diagnosis was confirmed by microscopical . . .

Pulmonary arteriovenous fistula: Angiocardiographic observations in nine cases

Pulmonary arteriovenous fistulas are hereditary hemangiomatous malformations of the pulmonary vascular bed. Almost 40 per cent of the reported cases also have hemangiomas elsewhere in the body, indicating that a close relationship to familial hemorrhagic telangiectasis (Rendu-Osier-Weber's disease) exists. When pulmonary arteriovenous fistulas are large and do not have systemic arterial connections, dyspnea, cyanosis, clubbing of the digits and polycythemia result from unsaturation of the blood. Hemoptysis may occur when there is rupture of the paper-thin pulmonary vascular anomaly. There is also a high incidence of cerebral symptoms due either to cerebral thrombosis, secondary to the polycythemia, or to infection, especially brain abscess. The heart remains normal in size because pulmonary arteriovenous fistulas do not cause increased pulmonary vascular resistance. In our series of nine cases the classical syndrome of cyanosis, clubbing of digits, polycythemia and a vascular murmur heard over the pulmonary fistula was present in one case only. One patient with dyspnea, fatigue and familial telangiectasis had bilateral pulmonary arteriovenous fistulas; chronic anemia prevented intense cyanosis and polycythemia. In three instances the patients were asymptomatic; in two the pulmonary arteriovenous fistula was an incidental finding; in the remaining two, acute cerebral conditions (brain abscess and meningoencephalitis) were the presenting symptoms. Vascular bruits were heard in eight patients. All patients had abnormal chest roentgenograms. The diagnosis of pulmonary arteriovenous fistula can often be made by conventional roentgenography, particularly if the index of suspicion is high. Pulmonary densities with hilar vascular connections localized in lobes or segments of the lung, or increased hilar vascularities, should arouse suspicion of an arteriovenous fistula. Change in size of the lesions after respiratory maneuvers (Valsalva, Müller) and delineation of the afferent arterial and efferent venous connections by body section radiography may be confirmatory. Angiocardiography, however, establishes the diagnosis and is recommended for preoperative evaluation. The treatment of pulmonary arteriovenous fistulas is surgical excision, with preservation of as much lung tissue as possible in order to preserve pulmonary function, especially if multiple lesions are present. Surgery is usually curative. It is recommended by some even in the asymptomatic case since the risk of brain abscess, fatal hemoptysis or development of cerebral thrombosis when polycythemia occurs is far greater than the morbidity and mortality of lobectomy or segmental resection.