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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anticholinergic syndrome (AS) due to accidental poisoning is exceptional. Mandragora contains a high concentration of atropine, hiosciamine and scopolamine. We have evaluated 15 patients with AS due to poisoning by Mandragora autumnalis, distributed in two family groups. The latency period since the ingestion was 1-4 hours (Means = 2.7 +/- 0.9). The clinical features corresponded to an AS of variable severity. All patients had blurred vision and dryness of mouth, nine (60%) had difficult micturition, nine dizziness, nine headache, eight (53%) vomit, two difficult swallowing and two abdominal pain. There was no correlation between the latency period and the clinical severity. Blushing, areactive mydriasis and tachycardia were found in all, dry skin and mucosae in 14 (93%), hyperactivity/hallucination in 14 and agitation/delirium in nine (60%). One patient developed a florid psychotic episode. Prostigmine (2-6 mg) was administered to 11 patients and physostigmine (0.5-2 mg) to six. The time until a definite response was observed was variable (3-36 hours). The patients treated with physostigmine had a better reversal of the psychoneurological symptoms. Mandragora was identified intermingled with chard [correction of stalwort] (Beta vulgaris) and spinach (Spinacia oleracea) leaves, and atropine and hiosciamine were identified.
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PMID:[Atropine poisoning by Mandragora autumnalis. A report of 15 cases]. 208 9

Some aspects of typhoid fever in 77 children are discussed. There were 48 boys and 29 girls and their ages ranged from 1 month to 12 years. The patients were treated with chloramphenicol 100 mg/kg/d during the first 2 weeks and with either amoxycillin (100 mg/kg/d) or ampicillin (200 mg/kg/d) during the third week. The average duration of fever was 5.2 days. There was 1 relapse and 1 child, a baby aged 1 month, died. The correct diagnosis was not suspected by the referring doctor in 38% of the patients. On admission the commonest complaints were fever, abdominal pain, diarrhoea, headache and vomiting. The commonest findings on examination were tenderness or distension of the abdomen, apathy or delirium, rhonchi or crepitations, liver enlargement and meningism. There was anaemia (Hb less than 10 g/dl) in 23% and lymphopenia (less than 1500/microliter) in 43% of the patients. The differential white blood cell count revealed 5% or more unsegmented neutrophils in 32% of the patients, while 25% had 10% or more band cells. Two patients (sisters) failed to respond after 15 and 16 days of therapy with chloramphenicol and ampicillin because of resistant Salmonella typhi and were successfully treated with co-trimoxazole. Practitioners caring for black patients should always be on the alert for typhoid fever; some patients may not respond to chloramphenicol or amoxicillin. During the acute phase milk feeds are best replaced by soya products because of abdominal distension or aggravation of diarrhoea by milk.
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PMID:[Aspects of typhoid fever in children]. 376 9

Bacillary dysentery, an acute infection caused by various strains of Shigella, is characterized by abdominal pain, tenesmus, and diarrhea with mucus, pus and blood. Neurologic manifestations including meningismus, delirium and convulsions may accompany the infection. We describe a thirteen-year-old girl who presented with headache, convulsion and loss of consciousness at the onset and developed diarrhea with blood and pus after hospitalization. The diagnosis of shigellosis was based on clinical data and isolation of the microorganism in the stool specimen. After improved physical functions, the patient developed mutism that continued for two days in the course of her illness, despite having no history of neurologic or psychological problems. She was diagnosed by a psychiatrist with organic mental syndrome NOS (Not Otherwise Specified) according to DSM-III-R criteria. None of the conditions that may cause mutism could be confirmed. This is the first reported case of mutism accompanying shigellosis.
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PMID:A case of childhood shigellosis with mutism. 856 Jun 15

Acute intermittent porphyria mimics a variety of commonly occurring disorders and thus poses a diagnostic quagmire. Psychiatric manifestations include hysteria, anxiety, depression, phobias, psychosis, organic disorders, agitation, delirium, and altered consciousness ranging from somnolence to coma. Some patients develop psychosis similar to schizophrenia. Psychiatric hospitals have a disproportionate number of patients with this disorder as only difficult and resistant patients accumulate there. Presence of photosensitive porphyrins in the urine is diagnostic. When porphyrins are absent, excess of alpha aminolevulinic acid and porphobilinogen are present in the urine. The definitive test is to measure monopyrrole porphobilinogen deaminase in RBCs. This diagnosis should be entertained in the following situations: (a) unexplained leukocytosis; (b) unexplained neuropathy; (c) etiologically obscure neurosis or psychosis; (d) 'idiopathic' seizure disorder; (e) unexplained abdominal pain; (f) conversion hysteria, and (g) susceptibility to stress. Porphyria is important in psychiatry as it may present with only psychiatric symptoms; it may masquerade as a psychosis and the patient may be treated as a schizophrenic person for years; the only manifestation may be histrionic personality disorder which may not receive much attention. Diagnosis is based on a high index of suspicion and appropriate investigation. Various psychotropic drugs exacerbate acute attacks. While it is important not to use the unsafe drugs in porphyric patients, it is also imperative to look for this diagnosis in cases where these drugs produce unprecedented drug reactions.
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PMID:Porphyria: reexamination of psychiatric implications. 865 42

A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. Promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.
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PMID:Neuroleptic malignant syndrome due to promethazine. 1054 78

A 21-year-old male soldier was admitted due to a sore throat, headache, generalized lymphadenopathy and persistent fever for 12 days. Despite empirical antibiotic treatment for four days at a clinic prior to admission, he continued to have persistent abdominal pain over his right upper quadrant region and progressive jaundice was followed by shock. After admission, he developed an episode of clonic seizures and became delirious and agitated. An electrocardiogram showed first degree atrioventricular (AV) block and non-specific ST-T wave changes. Hematological studies revealed thrombocytopenia, hypofibrinogenemia, abnormal partial thromboplastin time (PTT) and a positive test for D-dimer. The cerebrospinal fluid analysis showed pleocytosis with white cells of 84/mm3 with a lymphocyte predominance, protein of 97 mg/dL and glucose of 79 mg/dL. Indirect immunofluorescence assay showed a fourfold rise in antibodies to Orientia tsutsugamushi in paired serum with IgM antibody titer of 1:640. The patient had a favorable response after parenteral chloramphenicol in addition to oral tetracycline. Early ricognition of scrub typhus and early prescription of anti-rickettsial agents prevent complications of central nervous system involvement and further deterioration of cardiac and hematological function.
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PMID:Meningoencephalitis, myocarditis and disseminated intravascular coagulation in a patient with scrub typhus. 1156 71

In addition to pain, patients who are approaching the end of life commonly have other symptoms. Unless contraindicated, prophylaxis with a gastrointestinal motility stimulant laxative and a stool softener is appropriate in terminally ill patients who are being given opioids. Patients with low performance status are not candidates for surgical treatment of bowel obstruction. Cramping abdominal pain associated with mechanical bowel obstruction often can be managed with morphine (titrating the dosage for pain) and octreotide. Delirium is common at the end of life and is frequently caused by a combination of medications, dehydration, infections or hypoxia. Haloperidol is the pharmaceutical agent of choice for the management of delirium. Dyspnea, the subjective sensation of uncomfortable breathing, is often treated by titration of an opioid to relieve the symptom; a benzodiazepine is used when anxiety is a component of the breathlessness.
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PMID:Management of common symptoms in terminally ill patients: Part II. Constipation, delirium and dyspnea. 1157 23

A 33-year-old man with a history of recreational benztropine abuse presented to the emergency department with confusion, abdominal pain, and distention. An abdominal radiograph revealed gross fecal loading. He was initially treated with intravenous fluids and opiate analgesia. Subsequently, a diagnosis of anticholinergic poisoning was made, based on tachycardia, delirium, dry mucosa, and reduced bowel sounds. Treatment with tacrine reversed the delirium, and a history of repeated benztropine use was obtained. Persistent ileus was treated with repeated doses of neostigmine, and gastrointestinal motility returned with prompt defecation. Neostigmine appears to be useful in reversing ileus caused by anticholinergic drug overdose. Theoretically, it may be useful in reversing anticholinergic ileus resulting from acute drug overdose, allowing or enhancing decontamination, but the safety and potential efficacy of neostigmine in this scenario have not been established.
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PMID:Treatment of anticholinergic-induced ileus with neostigmine. 1171 51

We report on the case of a 20 year old woman with no previous psychiatric history, who displayed a first episode of catatonia with acute onset. Symptoms started plainly with sudden general impairment, intense asthenia, headache, abdominal pain and confusion. After 48 hours, the patient was first admitted to an emergency unit and transferred to an internal medicine ward afterwards. She kept confused. Her behaviour was bizarre with permanent swinging of pelvis, mannerism, answers off the point and increasingly poor. The general clinical examination was normal, except for the presence of a regular tachycardia (120 bpm). The paraclinical investigations also showed normal: biology, EEG, CT Scan, lumbar puncture. Confusion persisted. The patient remained stuporous, with fixed gazing and listening-like attitudes. She managed to eat and move with the help of nurses but remained bedridden. The neurological examination showed hypokinaesia, extended hypotonia, sweating, urinary incontinence, bilateral sharp reflexes with no Babinski's sign and an inexhaustible nasoorbicular reflex. The patient was mute and contrary, actively closed her eyes, but responded occasionally to simple instructions. For short moments, she suddenly engaged in inappropriate behaviors (wandering around) while connecting back to her environment answering the telephone and talking to her parents. The patient's temperature rose twice in the first days but with no specific etiology found. During the first 8 days of hospitalization, an antipsychotic treatment was administered: haloperidol 10 mg per os daily and cyamemazine 37.5 mg i.m. daily. Despite these medications, the patient worsened and was transferred to our psychiatric unit in order to manage this catatonic picture with rapid onset for which no organic etiology was found. On admission, the patient was stuporous, immobile, unresponsive to any instruction, with catalepsy, maintenance of postures, severe negativism and refusal to eat. A first treatment by benzodiazepine (clorazepate 20 mg i.v.) did not lead to any improvement. The organic investigations were completed with cerebral MRI and the ruling out of a Wilson's disease. Convulsive therapy was then decided. It proved dramatically effective from the first attempt; 4 shocks were carried out before the patient's relatives ask for her discharge from hospital. The patient revealed she had experienced low delirium during her catatonic state. The clinical picture that followed showed retardation with anxiety. She was scared with fear both for the other patients and the nursing team. She kept distant and expressed few affects. The treatment at the time of discharge was olanzapine 10 mg per os. She was discharged with a diagnosis of catatonia but with no specific psychiatric etiological diagnosis associated. She discontinued her follow-up a few weeks later. After one year, we had no information about her. Catatonia has now become rare but remains a problem for clinicians. We reviewed data concerning short term vital prognosis and psychiatric long term prognosis in catatonia. Lethal catatonia is associated with acute onset, both marked psychomotor and neurovegetative symptoms. In the light of literature, there is no proband clinical criterion during the episode that is of relevant diagnostic value to ascertain the psychiatric etiology.
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PMID:[Catatonia de novo, report on a case: immediate vital prognosis and psychiatric prognosis in longer term]. 1264 Mar 30

A woman, thyroidectomised because of a thyroid papillary carcinoma, interrupted temporarily her levothyroxine intake in order to be subjected to an extension study five weeks later. To minimise her symptoms for the first three weeks, a treatment was prescribed consisting of one 25 micro g-capsule of triiodothyronine every 8 hours. Nine days later she complained of abdominal pain, nausea, vomiting, fever of 40 degrees C and chest discomfort. A serum total triiodothyronine of 575.2 nmol/l was measured by chemoluminiscent immunoassay eleven hours after the intake of the latest capsule (normal level: 1.1-2.9 nmol/l). Along the following ten days the patient suffered from delirium, agitation, tachycardia, hypertension, constipation and later diarrhoea, but neither arrythmias nor axillary temperature over 38 degrees C. Fifty-nine measurements of the serum total triiodothyronine were performed in order to determine the kinetics of elimination of this drug. We estimate that the maximal serum concentration after the intake of the latest capsule could be 794.3 nmol/l, i.e. 397 times higher than the mean normal value. The elimination half-life was 24 hours 40 minutes. The charcoal haemoperfusion had no impact on the velocity of elimination. The concentration of triiodothyronine became normal 200 hours after the intake of the latest capsule, but the clinical manifestations still lasted three days more. The pharmacokinetic data suggest that this intoxication could be due to the intake of capsules containing 5 mg of triiodothyronine, i.e. a dose 200 times higher than that prescribed by her physician.
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PMID:[Triiodothyronine intoxication. A clinical and phamacokinetic study]. 1469 84


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