Dangerous mistake: an accidental caffeine overdose.

Caffeine (1,3,7-trimethylxanthine) is a natural product commonly presented in food's composition, beverages and medicinal products. Generally, it is thought to be safe under normal dosage, yet it can be fatal in case of severe intoxication. We report a case of a healthy 32-year-old woman who went to the local emergency department (ED) 30 min after ingesting, accidentally, 5000 mg of anhydrous caffeine for a preworkout supplement. At the ED, she presented an episode of presyncope followed by agitation. ECG showed polymorphic broad complex QRS tachycardia and arterial blood gas revealed metabolic acidaemia with severe hypokalemia. The dysrhythmia was successfully treated with intravenous propranolol. Acid-base and hydroelectrolytic disorders were also corrected. A persistent sinus tachycardia was observed in the first 2 days in the ward and 5 days later she was discharged asymptomatic with internal medicine follow-up.

Management of pulmonary embolism after recent intracranial hemorrhage: A case report.

RATIONALE: Venous thromboembolism may result from prolong immobilization following intracerebral hemorrhage. Massive pulmonary embolism with associated right heart failure is life-threatening, requiring treatment with anticoagulants or even thrombolytic agents. However, these drugs are contraindicated after a recent hemorrhagic episode, as they may induce further hemorrhage. There are no guidelines for treatment in these circumstances. PATIENT CONCERNS: A 57-year-old man experienced massive pulmonary embolism and shock 18 days after an intracerebral hemorrhage. DIAGNOSES: Tachycardia and high D-dimer (21.27 mg/L fibrinogen-equivalent units) were noted. Chest computed tomography showed bilateral pulmonary trunk embolism. INTERVENTIONS: Heparinization were used and activated partial thromboplastin time therapeutic range was 50 to 70 seconds. Fortunately, shock status and shortness of breath improved two days later. Continuing high dose Rivaroxaban was administrated for three weeks. OUTCOMES: There was no recurrent intracranial hemorrhage (ICH) following treatment for three-weeks with high-dose and one-year with standard dose of rivaroxaban. This report presents a treatment option in the management of these difficult clinical situations. LESSONS: The combination of unfractionated heparin infusion and continuing non-Vitamin K antagonist oral anticoagulants use could manage life-threatening pulmonary embolism following recent ICH. Theoretically, the use of NOAC is a safer strategy if the patient with previous history of major ICH.

A Fatal Case of Amlodipine Toxicity Following Iatrogenic Hypercalcemia.

Using calcium salts in management of amlodipine overdose is challenging. A 25-year-old male with known history of adult polycystic kidney disease presented with hypotension, tachycardia, and intact neurological status after ingestion of 450 mg of amlodipine. Immediately, normal saline infusion and norepinephrine were initiated. Two grams of calcium gluconate was injected, followed by intravenous infusion of 1.16 mg/kg/h. The patient was put on insulin-glucose protocol to maintain euglycemia and hyperinsulinemia. Electrocardiography demonstrated junctional rhythm. Serum creatinine was 2.5 mg/dL with metabolic acidosis. By the end of 24 h post-admission, his consciousness, blood pressure, and urine output were normal. Almost 32 h post-admission, he became disoriented and his oxygen saturation decreased and therefore was mechanically ventilated. Second chest X-ray showed pulmonary edema. Serum calcium level increased to 26.1 mg/dL. Calcium was discontinued, and furosemide infusion and calcitonin were intravenously administrated. Urine output increased and hemodialysis improved pulmonary edema and serum calcium level with no change in consciousness. Three days after admission, the patient became anuric and developed multi-organ failure and died 5 days post-admission. To avoid the consequences of excessive infusion of calcium in renal failure patients, the minimum calcium dose with close monitoring is recommended.

Successful management of minoxidil toxicosis in a dog.

CASE DESCRIPTION A 2-year-old sexually intact female mixed-breed dog was evaluated at an emergency hospital approximately 5 hours after ingestion of an unknown amount of over-the-counter topical hair growth promoter containing 5% minoxidil foam. Vomiting and signs of lethargy were reported by the owner, and physical examination revealed tachycardia and hypotension. No treatments were performed, and the dog was transferred to a veterinary referral hospital for management of suspected minoxidil toxicosis. CLINICAL FINDINGS On arrival at the referral hospital, the dog was tachycardic (heart rate, 200 to 220 beats/min) and hypotensive (systolic arterial blood pressure, 70 mm Hg). Electrocardiography revealed a regular, narrow-complex tachycardia with no evidence of ventricular ectopy. TREATMENT AND OUTCOME Hypotension was effectively managed with a constant rate infusion of dopamine hydrochloride (12.5 µg/kg/min [5.7 µg/lb/min], IV). Once normotensive, the dog remained tachycardic and a constant rate infusion of esmolol hydrochloride (40 µg/kg/min [18.2 µg/lb/min], IV) was initiated for heart rate control. A lipid emulsion was administered IV as a potential antidote for the toxic effects of the lipophilic minoxidil, with an initial bolus of 1.5 mL/kg (0.7 mL/lb) given over 15 minutes followed by a continuous rate infusion at 0.25 mL/kg/min (0.11 mL/lb/min) for 60 minutes. While hospitalized, the dog also received maropitant citrate and ondansetron. Resolution of clinical signs was achieved with treatment, and the dog was discharged from the hospital 36 hours after admission. Four days later, the owner reported that the dog had made a full recovery and had returned to its typical behavior and activity level at home. CLINICAL RELEVANCE To the authors' knowledge, this is the first report of successful clinical management of accidental minoxidil toxicosis in a dog.

Isolated limb perfusion with cytostatic drug leakage. / Perfusión aislada de extremidad inferior con fuga de quimioterapéutico.

Isolated limb perfusion is the treatment of stage III melanoma with in-transit metastasis. This technique allows the administration of cytostatics at an effective concentration and temperature, which could not be administered systemically because of their toxicity. The toxicity due to leakage of the chemotherapy agent from the limb into the systemic circulation is the most serious short-term complication, and is manifested by a systemic inflammatory response syndrome in the immediate post-intervention period. Early detection of this complication and its peri-operative management requires a multidisciplinary approach, in which the anaesthesiologist plays a key role. A case of isolated lower limb perfusion is reported in which the procedure had to be interrupted due to the passage of tumour necrosis factor into the systemic circulation, with severe intra-operative haemodynamic repercussions.

Clinical Features and Sites of Ablation for Patients With Incessant Supraventricular Tachycardia From Concealed Nodofascicular and Nodoventricular Tachycardias.

OBJECTIVES: This study sought to describe the clinical features and sites of successful ablation for incessant nodofascicular (NF) and nodoventricular (NV) tachycardias. BACKGROUND: Incessant supraventricular tachycardias have been associated with tachycardia-induced cardiomyopathies and have been previously attributed to permanent junctional reciprocating tachycardias, atrial tachycardias, and atrioventricular nodal re-entrant tachycardias. Incessant concealed NF and NV tachycardias have not been described previously. METHODS: Three cases of incessant concealed NF and NV re-entrant tachycardias were identified from 2 centers. RESULTS: The authors describe 3 cases with incessant supraventricular tachycardia resulting from NV (2 cases) and NF (1 case) pathways. Atrioventricular nodal re-entrant tachycardia was excluded by His synchronous premature ventricular complexes that either delayed or terminated the tachycardia. Ventricular pacing showed constant and progressive fusion in cases 1 and 3. In 2 cases, there was spontaneous initiation with a 1:2 response (cases 1 and 3); the presence of retrograde longitudinal dissociation or marked decremental pathway conduction in cases 1 and 3 sustains these tachycardias. The NV pathway was successfully ablated in the slow pathway region in case 3 and at the right bundle branch in case 1. The NF pathway was successfully ablated within the proximal coronary sinus in case 2. CONCLUSIONS: This is the first report of incessant supraventricular tachycardia using concealed NF or NV pathways. These tachycardias demonstrated spontaneous initiation from sinus rhythm with a 1:2 response and retrograde longitudinal dissociation or marked decremental pathway conduction. Successful ablation was achieved at either right-sided sites or within the coronary sinus.

Intralipid in acute caffeine intoxication: a case report.

Caffeine is arguably the most widely used stimulant drug in the world. Here we describe a suicide attempt involving caffeine overdose whereby the patient's severe intoxication was successfully treated with the prompt infusion of Intralipid. A 19-year-old man was found in an agitated state at home by the volunteer emergency team about 1 h after the intentional ingestion of 40 g of caffeine (tablets). His consciousness decreased rapidly, followed quickly by seizures, and electrocardiographic monitoring showed ventricular fibrillation. Advanced life support maneuvers were started immediately, with the patient defibrillated 10 times and administered 5 mg epinephrine in total and 300 + 150 mg of amiodarone (as well as lidocaine and magnesium sulfate). The cardiac rhythm eventually evolved to asystole, necessitating the intravenous injection of epinephrine to achieve the return of spontaneous circulation. However, critical hemodynamic instability persisted, with the patient's cardiac rhythm alternating between refractory irregular narrow complex tachycardia and wide complex tachycardia associated with hypotension. In an attempt to restore stability we administered three successive doses of Intralipid (120 + 250 + 100 mg), which successfully prevented a severe cardiovascular collapse due to a supra-lethal plasma caffeine level (>120 mg/L after lipid emulsion). The patient survived without any neurologic complications and was transferred to a psychiatric ward a few days later. The case emphasizes the efficacy of intravenous lipid emulsion in the resuscitation of patients from non-local anesthetic systemic toxicity. Intralipid appears to act initially as a vehicle that carries the stimulant drug away from heart and brain to less well-perfused organs (scavenging mechanism) and then, with a sufficient drop in the caffeine concentration, possibly as a tonic to the depressed heart.

Therapeutic Effects of Procainamide on Endotoxin-Induced Rhabdomyolysis in Rats.

Overt systemic inflammatory response is a predisposing mechanism for infection-induced skeletal muscle damage and rhabdomyolysis. Aberrant DNA methylation plays a crucial role in the pathophysiology of excessive inflammatory response. The antiarrhythmic drug procainamide is a non-nucleoside inhibitor of DNA methyltransferase 1 (DNMT1) used to alleviate DNA hypermethylation. Therefore, we evaluated the effects of procainamide on the syndromes and complications of rhabdomyolysis rats induced by lipopolysaccharide (LPS). Rhabdomyolysis animal model was established by intravenous infusion of LPS (5 mg/kg) accompanied by procainamide therapy (50 mg/kg). During the experimental period, the changes of hemodynamics, muscle injury index, kidney function, blood gas, blood electrolytes, blood glucose, and plasma interleukin-6 (IL-6) levels were examined. Kidneys and lungs were exercised to analyze superoxide production, neutrophil infiltration, and DNMTs expression. The rats in this model showed similar clinical syndromes and complications of rhabdomyolysis including high levels of plasma creatine kinase, acute kidney injury, hyperkalemia, hypocalcemia, metabolic acidosis, hypotension, tachycardia, and hypoglycemia. The increases of lung DNMT1 expression and plasma IL-6 concentration were also observed in rhabdomyolysis animals induced by LPS. Treatment with procainamide not only inhibited the overexpression of DNMT1 but also diminished the overproduction of IL-6 in rhabdomyolysis rats. In addition, procainamide improved muscle damage, renal dysfunction, electrolytes disturbance, metabolic acidosis, hypotension, and hypoglycemia in the rats with rhabdomyolysis. Moreover, another DNMT inhibitor hydralazine mitigated hypoglycemia, muscle damage, and renal dysfunction in rhabdomyolysis rats. These findings reveal that therapeutic effects of procainamide could be based on the suppression of DNMT1 and pro-inflammatory cytokine in endotoxin-induced rhabdomyolysis.

[Cardiogenic shock after drug therapy for atrial fibrillation with tachycardia : Case report of an 89-year-old woman]. / Kardiogener Schock nach bradykardisierender Therapie bei tachykardem Vorhofflimmern : Fallvorstellung einer 89-jährigen Patientin.

ß-Blockers and calcium channel blockers are commonly used drugs in the treatment of atrial fibrillation with tachycardia. However, in patients with high myocardial susceptibility and vulnerability, combination therapy with ß-blockers and non-dihydropyridine calcium channel blockers (verapamil or diltiazem) but also individual administration can cause drug-induced cardiogenic shock. Thus, the simultaneous administration of ß-blockers and non-dihydropyridine calcium channel blockers is absolutely contraindicated. In case of acute heart failure, isolated application is also contraindicated. In the treatment of a cardiogenic shock induced by ß-blockers and/or non-dihydropyridine calcium channel blockers, administration of intravenous calcium, glucagon or high-dose insulin is recommended.

[High-dose magnesium sulfate in the treatment of aconite poisoning]. / Hochdosiertes Magnesiumsulfat bei Aconitumintoxikation.

This article reports the case of a 62-year-old male patient who ingested the roots of Monkshood (Aconitum napellus) and white hellebore (Veratrum album) dissolved in alcohol with a suicidal intention and suffered cardiotoxic and neurotoxic symptoms. After contacting the Poison Information Centre ventricular arrhythmia was treated with high-dose magnesium sulphate as the only antiarrhythmic agent and subsequently a stable sinus rhythm could be established after approximately 3 h. Aconitum napellus is considered the most poisonous plant in Europe and it is found in gardens, the Alps and the Highlands. Poisoning is mainly caused by the alkaloid aconite that leads to persistent opening and activation of voltage-dependent sodium channels resulting in severe cardiac and neurological toxicity. As no specific antidote is known so far, poisoning is associated with a high mortality. The therapy with high-dose magnesium sulphate is based on in vitro and animal experiments as well as limited clinical case reports.

[Drug-induced magnesium deficiency]. / Magnesium-Mangel und Arzneimittel.

A lot of drugs can induce hypomagnesemia as side effect. On the other hand, magnesium deficiency may be a risk factor for digitalis and drugs known to prolong the QT-interval and thus favour the development of torsades-de-pointes tachycardias. Controversely, the indication for most oral magnesium supplements in Germany is: proven magnesium deficiency if this is the cause for muscular troubles (neuromuscular disturbances, calf cramps). Due to this cutback magnesium attracts poor attention in clinical practice and the determination of serum magnesium concentrations is seldom ordered. Moreover, the lower level of the reference range for serum magnesium is often kept too low. As a consequence hypomagnesemia as side effect remains frequently undetected.

Baicalein, an active component of Scutellaria baicalensis Georgi, improves cardiac contractile function in endotoxaemic rats via induction of heme oxygenase-1 and suppression of inflammatory responses.

AIM OF THE STUDY: To evaluate the protective effect of baicalein on myocardial dysfunction caused by endotoxaemia in rats and to explore the possible mechanisms. MATERIALS AND METHODS: Baicalein (10mg/kg, intravenous) was administered to conscious Wistar rats 30min after lipopolysaccharide (LPS; 10mg/kg, intravenous) challenge. Six hours after LPS administration, the contractile function of the isolated heart was examined using the Langendorff technique. Cardiac protein expression related to inflammatory responses, superoxide anion production and caspase-3 activity were measured. RESULTS: Post-treatment with baicalein significantly attenuated the LPS-induced hypotension with accompanying tachycardia. The contractile function of isolated heart was significantly preserved 6h after LPS administration, following treatment with baicalein. Furthermore, baicalein induced the expression of heme oxygenase-1 protein and reduced superoxide anion formation in the myocardium of LPS-treated rats. Cardiac levels of inducible nitric oxide synthase, monocyte chemoattractant protein-1, phospho-IκBα and phospho-p65 protein and caspase-3 activity significantly increased 6h after LPS challenge but baicalein significantly attenuated these LPS-induced changes. CONCLUSIONS: Baicalein improves myocardial contractility in LPS-induced sepsis, which may be related to reductions in oxidative stress, myocardial inflammatory responses and apoptosis.

Analysis of the anatomical tachycardia circuit in verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node.

BACKGROUND: Calcium channel-dependent tissue has been suggested to be involved in the circuit of verapamil-sensitive atrial tachycardia originating from the atrioventricular (AV) node vicinity (V-AT), but little information exists. METHODS AND RESULTS: To examine the tachycardia circuit of V-AT, a single extrastimulus was delivered during tachycardia to 10 sites of the intraatrial septum: the earliest atrial activation site; His bundle (HB) site; 3 arbitrarily divided sites on the AV junction extending from the HB site to the coronary sinus ostium (CSOS) (sites S, M, and I); the internal-CSOS, inferior-CSOS, superior-CSOS, posterior-CSOS, and posteroinferior-CSOS in 10 patients with V-AT. The longest coupling interval that reset V-AT and subsequent return cycle were measured. The longest coupling interval at earliest atrial activation site was significantly longer than the longest coupling interval at the HB site, site S, M, and I, internal-CSOS, inferior-CSOS, superior-CSOS, posterior-CSOS, and posteroinferior-CSOS, respectively (P<0.001 for HB site and P<0.0001 for the remaining 8 sites). The return cycle at earliest atrial activation site did not differ from the tachycardia cycle length, whereas those at the remaining 9 sites were significantly longer than tachycardia cycle length (P<0.001). Furthermore, a single extrastimulus delivered from sites inferior to the HB site advanced His potential without resetting V-AT in 7 patients in whom AV block was not observed during tachycardia. CONCLUSIONS: Atrial tissue within the Koch's triangle extending from the HB site to posteroinferior-CSOS is not involved in the tachycardia circuit. Verapamil-sensitive atrial tissue close to the AV node but not the AV nodal conducting system forms the tachycardia circuit of V-AT.

Infants and children with tachycardia: natural history and drug administration.

Tachyarrhythmias can occur at any age from the developing fetus through adulthood. However, in deference to adult-onset ischemic cardiac issues, abnormal heart rhythms occurring in the young are often due to developmental alterations of the cardiac conduction tissue, genetically-inherited changes of myocardial cellular ion membrane properties and both pre- and post-surgical repair of associated structural congenital heart anatomical defects. And different from adults, abnormal rhythms occurring in the young can spontaneously disappear with progressive patient growth. Both supra- and ventricular tachyarrhythmias occur in the young although atrial rhythm abnormalities far exceed those of the ventricle. In both, pharmacologic therapies to alter tissue conduction and refractoriness remain the mainstay for initial intervention in the infant and young child, reserving more invasive and potentially harmful ablation therapies for drug-refractory cases. The purpose of the review is to present common and uncommon tachyarrhythmias which can occur in the fetus and throughout infancy. Emphasis will be placed on their electrocardiographic identification, recognition of any associated structural congenital heart defects and recommended pharmacologic management. Drug therapies will be divided according to mechanism of action and discussions of which particular agent is potentially best-suited to treat which specific tachyarrhythmia. A listing of current pharmacologic agents used in the young with appropriate dosages is included.

Potent oxindole based human beta3 adrenergic receptor agonists.

The synthesis and biological evaluation of a series of oxindole beta(3) adrenergic receptor agonists is described. A modulation of rat atrial tachycardia was observed with substitution at the 3-position of the oxindole moiety.

Transesophageal electrophysiologic study in children and young patients.

Transesophageal electrophysiologic study (TEEPS) is a semi-invasive method of atrial stimulation and recording. The aim of the study was to report our experience with TEEPS in children and young adults. A total of 153 TEEPS were performed in 147 consecutive patients aged between 26 days to 26 years (mean 9.8 years) with the following indications: evaluation of symptoms that may be signs of any arrhythmias in 89 procedures (Group A), risk assessment of Wolff-Parkinson-White syndrome (WPW) in 17 procedures (Group B), determination of the mechanism of previously detected or ongoing tachycardia on ECG or Holter monitoring in 22 procedures (Group C), assessment of antiarrhythmic therapy effectiveness in 17 procedures (Group D), and follow-up of radiofrequency ablation procedure (RFA) in 8 procedures (Group E). A similar pacing protocol was performed for induction of tachycardia in each patient. Tachycardia was induced in a total of 72 procedures (72/153, 47%): 32/89 (36%) in Group A, 13/17 (76.5%) in Group B, 12/22 (54.5%) in Group C, 12/17 (70.6%) in Group D and 3/8 (37.5%) in Group E. In Group A, the ventriculoatrial (VA) interval of inducible tachycardia was found to be shorter than 70 msec in 16/32 (50%) and longer than 70 msec in 12/32 (37.5%) patients and these patients were diagnosed as having atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT), respectively. In this group, 1 atrial tachycardia, 2 junctional ectopic tachycardia, 1 sinus node reentrant tachycardia and 1 permanent junctional reciprocating tachycardia (PJRT) were also diagnosed. In conclusion, transesophageal atrial stimulation is a valuable tool in the initial evaluation of patients with symptoms possibly related with arrhythmia or in the management of patients who have any arrhythmia.

Vasoactivity of bovine polymerized hemoglobin (HBOC-201) in swine with traumatic hemorrhagic shock with and without brain injury.

BACKGROUND: We previously reported that bovine polymerized hemoglobin (HBOC- 201) improved outcome in swine with hemorrhagic shock (HS) with and without traumatic brain injury (TBI). Herein, we add analyses of blood pressure (BP) responses, associated physiologic data, and HS fluid infusion guidelines. METHODS: HBOC-201 versus standard fluid resuscitation was compared in four anesthetized invasively monitored swine models: moderate controlled HS, severe controlled HS, severe uncontrolled HS (liver injury), and severe uncontrolled HS/TBI (liver/parietal brain injuries). Pigs received fluid for hypotension and tachycardia, and were followed up to 6 (HS alone) or 72 hours (HS/TBI). The change in mean arterial pressure (DeltaMAP) response severity was stratified and analyzed based on infusion number and HS severity, using Student's t and Fisher's exact tests. RESULTS: HBOC-201 vasoactivity resulted in higher MAP in all studies. Among HBOC-201 pigs, DeltaMAP responses were significant for the first two infusions and inversely related to HS severity. Among controls, DeltaMAP responses remained significant through the fourth infusion in controlled HS models, and through the first in severe uncontrolled HS/TBI; none were significant in severe uncontrolled HS. DeltaMAP was higher with HBOC-201 through the first infusion in moderate controlled HS, the fifth in severe uncontrolled HS, and the second in severe uncontrolled HS/TBI; there were no group differences in severe controlled HS. No severe MAP responses occurred. Higher DeltaMAP severity did not impact outcome. Hypotension satisfied fluid reinfusion criteria less consistently than tachycardia. Overall, HBOC-201 improved physiologic parameters and survival without causing hypoperfusion; in severe HS, perfusion improved. CONCLUSIONS: In swine with HS +/- TBI, HBOC-201 had mild to moderate vasoactivity, resulting in significant DeltaMAP responses mainly after initial infusions, no severe/adverse responses, and improved outcome. Our data suggest that use of physiologic parameters (e.g., tachycardia), in addition to hypotension to guide fluid reinfusion during HS resuscitation with HBOC-201, will minimize hypoperfusion risk and maximize potential benefit.