Cases reported "Hypotension"

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1/4. hypotension due to interaction between lisinopril and tizanidine.

    OBJECTIVE: To report a case in which significant hypotension occurred after initiation of tizanidine in a patient using the antihypertensive agent lisinopril. CASE SUMMARY: A 48-year-old woman was admitted due to cerebral hemorrhage at the midbrain and pons, with extension to the fourth ventricle. consciousness disturbance (glasgow coma scale 4) with a decerebrate posture improved 5 days after stroke onset. As the BP was fairly high, antihypertensive agents, including lisinopril, were initiated. Three weeks later, the decerebrate rigidity and high BP remained, and tizanidine was initiated to see whether the decrease in muscle tone could facilitate hypertension control and motor recovery. However, the BP dropped dramatically within 2 hours after the first dose of tizanidine. The tizanidine and all of the antihypertensive medications were withdrawn. Tizanidine was used again after her BP had stabilized, but did not produce similar problems. DISCUSSION: A similar event was reported in 2000. The reaction in our patient appeared after tizanidine initiation and improved after both lisinopril and tizanidine were discontinued. According to the Naranjo probability scale, this was classified as a possible drug interaction. This kind of reaction is seldom mentioned as occurring during co-administration with tizanidine. With its characteristics, tizanidine has the potential to compromise hemodynamic stability during concomitant angiotensin-converting enzyme inhibitor use. CONCLUSIONS: Based upon the literature review, the hypotension in this patient was possibly due to the interaction between tizanidine and lisinopril.
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2/4. Refractory anaphylactic shock associated with ketoconazole treatment.

    OBJECTIVE: To report a rare but severe reaction of refractory anaphylactic shock with ketoconazole treatment-associated hypotensive episodes in an elderly patient. CASE SUMMARY: A 72-year-old woman received antifungal therapy for her almost completely occluded cornea infected with candida albicans. She was initially prescribed oral ketoconazole 200 mg twice daily. She developed hypotension over the first 2 days of therapy (BP 136/82 mm Hg at baseline; 90/50 mm Hg on day 2). Severe hypotension (BP 90/49 mm Hg) unresponsive to fluid therapy or high-dose dopamine developed on day 4 of therapy. An invasive Swan-Ganz catheterization study showed a very low level of peripheral vascular resistance with high cardiac output index without clinical signs of infection. When laboratory tests showed a high level of plasma tryptase, anaphylactic redistribution shock was diagnosed. Her vital signs became more stable after treatment with hydrocortisone and epinephrine infusion. She was discharged in good condition after 24 hours of observation. DISCUSSION: As of December 2004, refractory anaphylactic shock resulting from ketoconazole use had not been reported. The events of hypotension were strongly associated with the intake of ketoconazole. The hemodynamic results obtained with Swan-Ganz catheterization were compatible with anaphylactic shock. The Naranjo probability scale showed a probable association of the adverse event with ketoconazole. CONCLUSIONS: ketoconazole may cause severe anaphylactic shock even when taken orally. Invasive catheterization and elevated tryptase levels can provide important information in the management of anaphylactic shock.
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3/4. Ziprasidone- and lithium-induced neuroleptic malignant syndrome.

    OBJECTIVE: To report a case of ziprasidone- and lithium-induced neuroleptic malignant syndrome (NMS). CASE SUMMARY: A 47-year-old white male with a history of schizoaffective disorder was admitted to the hospital due to an exacerbation of severe mania. He had been taking lithium 450 mg twice daily and divalproex sodium 750 mg/day. On hospital day 2, ziprasidone 80 mg twice daily was added, and as-needed doses of intramuscular ziprasidone 20 mg and lorazepam 2 mg were used for agitation. On day 6, the patient developed hyperthermia (39.4 degrees C), elevated creatine kinase 26,000 units/L and white blood cell (WBC) count (20.7 x 10(3)/microL), myoglobinuria, hypotension (68/40 mm Hg), altered mental status, and tachypnea (28 breaths/min). This case is notable for the absence of muscle rigidity, which presents in greater than 90% of patients with NMS taking traditional antipsychotics. DISCUSSION: This case of ziprasidone- and lithium-induced NMS is of probable cause, as determined by the Naranjo probability scale. The patient presented with symptoms consistent with NMS 4 days after initiation of ziprasidone and lithium. The majority of NMS cases present with the core features of hyperthermia, muscle rigidity, and elevated CK levels. Other frequently seen symptoms include altered mental status, tachypnea, tachycardia, elevated WBC count, hypotension, diaphoresis, and myoglobinuria. Our patient presented with 2 of the core symptoms, but did not develop muscle rigidity at any time. NMS criteria include muscle rigidity as one of the major presenting symptoms. Recent literature suggests that perhaps NMS due to novel antipsychotics presents with less muscle rigidity than is seen with traditional agents due to their lower affinity for the dopamine D2 receptor. CONCLUSIONS: This case illustrates that NMS due to the novel antipsychotic ziprasidone may present with many of the core symptoms of the syndrome, but possibly less muscle rigidity than is seen with traditional agents.
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4/4. Hypotonia during amikacin administration in a patient treated with continuous ambulatory peritoneal dialysis.

    In this report we present the history of a patient treated with continuous ambulatory peritoneal dialysis (CAPD) in whom episodes of hypotonia can be related to the administration of amikacin, an antibiotic from the aminoglycosides group. The 68-year-old female patient was admitted for initiation of renal replacement therapy with CAPD. Her renal failure was probably attributable to hypertension. Three days after catheter implantation, the patient reported dysuric symptoms, and a urine culture showed significant growth of escherichia coli. amikacin 250 mg and cefazolin 1.0 g were administered intravenously once daily in accordance with the antibiogram. On the third day of antibiotic administration, the patient fainted, showing an arterial blood pressure of 90/60 mmHg. On the subsequent 2 days, decreases of postural arterial blood pressure to between 90/60 mmHg and 80/50 mmHg were reported two or three times daily. The patient was treated with antibiotics for the next 6 days and felt very bad the entire time, with an arterial blood pressure of 80/50 mmHg. The patient's condition improved 2 days after discontinuation of treatment with antibiotics, and episodes of hypotonia stopped. The decrease in the arterial blood pressure observed in our patient during intravenous administration of amikacin can, with a high probability, be related to the calcimimetic activity of this aminoglycoside and the resulting inhibition of parathyroid secretion.
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