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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 45-year-old man ate about 10 gm of dapsone (DDS). After initial vomiting marked methemoglobinemia with cyanosis, headache, and confusion developed. Methemoglobinemia subsided 7 days after ingestion when the concentrations of DDS and monoacetyldapsone (MADDS) were at the therapeutic level. Signs of hemolysis appeared on the third day after DDS ingestion, the hemolysis being maximal more than one week after ingestion. The initial disappearance of DDS and MADDS was slow, the apparent half-lives being 88 and 67 hr, respectively. Peroral activated charcoal seemed to shorten the half-lives of DDS and MADDS markedly. This result supports the concept of the enterohepatic cycle of dapsone and recommends the use of activated charcoal for several days in acute poisonings caused by DDS.
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PMID:Acute dapsone intoxication: a case with prolonged symptoms. 43 85

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.
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PMID:Delayed sulfhemoglobinemia after acute dapsone intoxication. 715 40

Isobutyl nitrite has recently become a popularly abused drug in the United States. Although many adverse effects, including headache, hypotension, and methemoglobinemia, are known to occur following exposure to this class of drugs, little has been written concerning the effects of illicit use of isobutyl nitrite. In this case, severe tracheobronchitis developed following short-term exposure by inhalation of this drug.
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PMID:Severe tracheobronchitis from inhalation of an isobutyl nitrite preparation. 727 14

The efficacy of an oral 8-aminoquinoline (8-[[6-(diethylamino)hexyl]amino]-6-methoxy-4-methylquinoline) (WR6026) in the treatment of 16 patients with kala azar was evaluated. The first 8 patients received therapy for 2 weeks at a dosage of 0.75-1.00 mg/(kg.d); 1 patient was cured, and in regard to the other 7, a 1-logarithm decrease in the number of splenic parasites and clinical improvement were noted. The next 8 patients received therapy for 4 weeks at the same daily dosage (1 mg/[kg.d]); 4 were cured, and for the other 4, 1- to 2-log decreases in the number of parasites and clinical improvement (in regard to weight, liver and spleen size, hemoglobin level, and leukocyte count) were noted. The therapy was associated with minimal toxicity; adverse effects included gastrointestinal distress, headache, and methemoglobinemia. The fact that one-half of the patients were cured indicates that future trials with longer regimens and higher dosages are warranted and should include patients for whom existing treatment methods have failed.
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PMID:Phase 2 efficacy trial of an oral 8-aminoquinoline (WR6026) for treatment of visceral leishmaniasis. 788 30

In the paper a thorough study of the influence of the methemoglobin levels and the occurrence of certain syndromes of clinical symptoms was made in the inhabitants living in the immediate vicinity of the large refuse dumps. During a 2.5-day clinical hospitalization the following examinations were done: general medical, specialistic and neuropsychological examinations, biochemical-analytical examination, EKG, chest X-ray, USG of the abdominal cave, spirometric tests, toxicological investigation of body fluids: carboxyhemoglobin, methemoglobin, lactates. The air pollution was measured and included: continuous measurement of the suspended particulate matter, carbon monoxide, sulfur dioxide, nitrogen oxide, nitrogen dioxide and the sum of nitrogen oxides. The evaluation of the refuse dumps gas showed that its main compounds were: carbon dioxide, methane in the amount of a few volume percent. Other pollutants were: carbon monoxide, hydrogen sulfide, methane homologues and aromatic hydrocarbons. The results of biochemical investigations were within normal limit. The elevated methemoglobin levels were found in 8 patients. The increased values of blood lactate concentration were found in 14 people and in 8 people the elevation of carboxyhemoglobin level was noted. The results of toxicological investigation do not unequivocally indicate the occurrence of toxic methemoglobinemia. However, the elevated levels of methemoglobin and lactates indicate a slight degree of oxygen deficiency in the body. In the examined people typical symptoms of methemoglobinemia were not observed, the only symptoms which may indicate their impact on the central nervous system were frequent headaches and neurovegetative disorders.
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PMID:The frequency of toxic methemoglobinemias in people living in the vicinity of refuse dumps in Barycz. 871 Nov 89

Methemoglobinemia is a rare complication that can occur with the use of benzocaine-containing compounds. Two cases of methemoglobinemia are reported, and the pathophysiology and treatment of methemoglobinemia are reviewed. Both patients received topical 20% benzocaine spray before endoscopy. Immediately following the procedure, there was a reduction in O2 saturation assessed by pulse oximetry that was refractory to O2 therapy. Dramatic peripheral and central cyanosis developed. O2 saturation measured by pulse oximetry ranged from 83% to 87% on O2 by nasal prongs and 100% O2 by a nonrebreathing mask. Both patients were mildly confused and one patient complained of a significant headache. The diagnosis of methemoglobinemia was considered and arterial blood gas sampling was performed. In both patients, the arterial blood had a chocolate brown colour. A methemoglobin level of 48% and 18% was noted in patient 1 and patient 2, respectively. Both patients were treated with methylene blue, resulting in a significant improvement with gradual normalization of their O2 saturation within 10 min to 30 min. The use of benzocaine spray may not markedly alter the patient's perception of endoscopy and thus, the routine use of these agents should be questioned. If such agents are used, the physician must be aware of this association to prevent a delay in the diagnosis and management of this rare, but potentially lethal, condition.
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PMID:Benzocaine-induced methemoglobinemia: a condition of which all endoscopists should be aware. 1549 3

Acute ingestion of copper sulfate has been reported to cause gastrointestinal injury, hemolysis, methemoglobinemia, hepatorenal failure, shock; or even death. The toxicity of organocopper compounds, however, remains largely unknown. A 40-y-old man attempted suicide by ingesting some 50 ml of Sesamine fungicide. He immediately developed headache, vomiting and abdominal pain, followed by progressive dyspnea, cyanosis, dark urine and diarrhea. Severe methemoglobinemia and hemolysis were documented, and treatment with ascorbic acid and hydration was commenced. He was referred to our service 3 d later for methylene blue treatment. Despite the above treatment, his symptomatology persisted and it was not until 5 d post-ingestion that the implicated fungicide was identified as copper-8-hydroxyquinolate. BAL therapy and plasma exchange were instituted, which decreased his plasma hemoglobin from 1,300 mg/dL to 29.1 mg/dL, and lowered his methemoglobin level from 20.9% to 1.1%. His serum and urine copper concentration dropped from 238 microg/dL to 96 microg/dL and from 112 microg/dL to 16 microg/dL, respectively. He was discharged uneventfully 18 d post-ingestion. Pre-existing glucose-6-phosphate dehydrogenase (G6PD) deficiency as well as copper-induced inhibition of G6PD activity was documented during hospitalization. Organocopper compounds may cause prolonged hemolysis and methemoglobinemia through oxidative stress, especially among patients with G6PD deficiency. Antidotal therapy with methylene blue is not likely to be effective in this setting: treatment with intensive supportive measures and other therapeutic options, such as plasma exchange, should be sought.
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PMID:Prolonged hemolysis and methemoglobinemia following organic copper fungicide ingestion. 1558 50

Methemoglobinemia and hemolysis are the most prominent side-effects of exposure to a wide variety of arylamine drugs, including agricultural and industrial chemicals. Recent studies with aniline and dapsone have identified N-hydroxyl metabolites as the red blood cell (RBC) mediators. This study examines the time-course methemoglobinemic potential of several halogenated aniline phenylhydroxylamines. Symptoms of aniline poisoning include headache, fatigue, dizziness, respiratory and cardiac arrest, and possibly death. Initial studies indicated that the parent compounds are converted to their toxic metabolites (N-hydroxylamine), which enter the RBC and react with oxyhemoglobin. Consequent reduction of molecular oxygen to active oxygen species occurs, leading to RBC damage. Our laboratory is investigating the role of redox cycling and an alternative hypothesis--that a "hydroxylamine-centered" radical formed during arylhydroxylamine-oxyhemoglobin reaction results in RBC injury. The methemoglobinemic capacities of several structurally related N-hydroxy derivatives of aniline--phenylhydroxylamine (PHA), p-fluoro-, p-chloro-, p-bromo-, and p-iodo-PHA--were studied spectrophotometri-cally by treating washed rat RBC at concentrations ranging from 30 to 300 microM of the test compounds for up to 240 minutes. The results showed dose- and time-dependent changes in the induction of methemoglobin (MetHb) by aniline derivatives. The MetHb levels peaked to as high as 75% and remained elevated up to 240 minutes, depending on the electronegativity of halogenated phenylhydroxylamine aniline. This study supports the previous findings that there may be several aniline-derived metabolites other than PHA that are capable of inducing MetHb. The minimum dose required to induce this effect and duration of the MetHb may vary with the test agent.
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PMID:Aniline derivative-induced methemoglobin in rats. 1571 9

Benzocaine administration to facilitate upper endoscopic procedures can result in the relatively uncommon but potentially fatal complication known as methemoglobinemia. For this reason, the Veterans Health Administration (VA) announced on February 8, 2006, that they would stop using benzocaine-containing sprays for procedures involving the mouth and throat. Methemoglobinemia should be considered in any patient who demonstrates cyanosis, respiratory distress, headache, lightheadedness, and a dark, chocolate-colored blood after receiving pharyngeal anesthesia. Prompt recognition of this rare (but potentially fatal) condition is important. Once identified, treatment is generally rapid with methylene blue. The patient should be monitored in the intensive care setting for recurrence. Knowledge of this adverse medication reaction is essential for all gastroenterology nurses.
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PMID:Methemoglobinemia and benzocaine. 1804 3

There is a long list of prescribed and over the counter oxidizing agents that can induce methemoglobinemia. We report a case of methemoglobinemia in a 46-year-old man with a mayor depression disorder who ingested 30 pills of diphenhydramine, 30 pills of haloperidol, 20 pills of dolagesic, 20 pills of cyclobenzaprine, 20 pills of naproxen, 14 pills of cephalexin, and 48 pills of chlorzoxazone. On admission, he was on mechanical ventilation, and responded only to painful stimuli. Five hours later his face, hands and feet became cyanotic. The pulse oximetry revealed a Sp02 of 85%. The dark chocolate color arterial blood showed a Pa02 of 290.8 mm Hg and oxygen saturation (Sa02) of 99%. The chocolate color arterial blood and unchanged Sp02 suggested the diagnosis of methemoglobinemia. One mg per Klg of intravenous methylene blue was administered in 5 minutes. Twenty minutes later, the cyanosis began to fade and one hour later, it had disappeared and the Sp02 was 99%. Early treatment of methemoglobinernia is crucial in preventing tissue hypoxia. Methylene blue is the treatment of choice in symptomatic patients. The initial dose of methylene blue is 1-2 mg/kg of a 1% solution administered over 5 minutes. Reduction of methemoglobin is usually complete within 1 hour. If methemoglobinernia persists, a second dose not to exceed a total dose of 5-7 mg/kg may be administered. Because headache, nausea, vomiting, diarrhea, and angina may occur with therapeutic doses, methylene blue should only be administered to those patients with symptoms or signs of hypoxia.
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PMID:Methemoglobinemia: life-threatening hazard of multiple drug ingestions. 1960


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