Loss Of Pupillary Reflex Research Articles

Abstract 1122‐000171: Unusual Multicompartmental Intracranial Hemorrhage After Tenecteplase Administration

Introduction : The 2019 AHA/ASA updated Guidelines for the Early Management of Patients with Acute Ischemic Stroke mention tenecteplase (TNK) as a reasonable therapy in patients without contraindications for IV fibrinolysis who are also eligible to undergo mechanical thrombectomy. We describe a case of acute left MCA ischemic stroke treated with IV TNK (IV bolus of 0.25 mg/kg) followed by mechanical thrombectomy with subsequent multicompartmental intracranial hemorrhages unrelated to area of infraction. Methods : A retrospective review at a single center university hospital was performed for all intravenous TNK administrations outside of a clinical trial setting from October 2020 to July 2021. Results : A 61‐year‐old male with history of HTN and cardiomyopathy (EF<20%). Presented with sudden onset right sided weakness, aphasia and left gaze. Presenting NIHSS was 28. CT head with hyperdense left MCA sign and ASPECTS score of 10. CTA confirmed proximal left MCA M1 segment occlusion. IV TNK was given within 01:23 hours of symptoms onset. Subsequently, patient underwent emergent mechanical thrombectomy for disabling large vessel occlusion stroke. Spontaneous near complete recanalization of left MCA occlusion was noted on initial angiography run with small non flow limiting distal thrombi visualized in the distal MCA territories. Immediate post procedure CT head was negative for any intracranial hemorrhage. Patient’s exam was noted to improve to NIHSS of 2. Approximately 6 hours after the TNK administration, patient became acutely unresponsive with NIHSS of 26. With Glasgow Coma Scale 7 patient required emergent intubation. CT head revealed bilateral cerebellar intraparenchymal hemorrhages, extensive subarachnoid hemorrhage in basal cisterns and within the sulci in bilateral frontotemporal regions, as well as subdural hemorrhages along the falx and tentorial dural folds. Hypertonic saline was administered followed by emergent extraventricular drain placement. Tranexamic acid 1000 mg was given as emergent reversal, fibrinogen level was 155 mg/dL. Despite aggressive medical management and over following 24 hours, exam worsened with loss of pupillary reflexes. Patient was terminally extubated 2 days after initial presentation in accordance with his advance directives. Conclusions : Tenecteplase was a reasonable choice in this case given LVO and disabling stroke. The patient’s neurological exam improved significantly after TNK with evidence of spontaneous recanalization. However, patient’s multicompartmental intracranial hemorrhages unrelated to area of infraction were unusual in the absence of any vascular lesions to predispose hemorrhage based on CT and conventional angiography. Further observational studies are warranted to evaluate similar complications of Tenecteplase administration and their occurrence rates.

Commentary: Closantel - A lesser-known evil.

Closantel is an antiparasitic agent routinely used in veterinary practice against some parasites of livestock. It is not used against agricultural and household pests. Recently, it has been discovered that closantel also acts against Onchocerca volvulus, a filarial nematode causing river blindness in humans.[1] Closantel belongs to the chemical class of the salicylanilides, which acts as an uncoupler of oxidative phosphorylation in the cell mitochondria and disturbs ATP production. This impairs the parasite's motility and probably other processes as well. Closantel also disturbs the liquid and ion transport mechanisms in the parasite's membranes. Closantel is a narrow-spectrum anti-helminthic effective against a few roundworms (mainly blood-sucking species), against flukes (e.g., Fasciola hepatica) and also against certain myiasis. It is ineffective against tapeworms or most external parasites. It is not used in swine, poultry, horses, or pets. It is used moderately in ruminants both as an injectable or a drench, often mixed with other anti-helminthics. After oral administration, closantel is readily absorbed into the bloodstream. Four days after treatment up to 60% of the injected and 30% of the drenched closantel is absorbed to blood. In the blood, >99% of the unchanged closantel binds strongly to plasma albumins. Peak plasma levels are reached between 10 and 48 h after administration, both after oral or intramuscular administration. Half-life in plasma is 3 to 4 weeks. Owing to the strong binding to plasma albumins, closantel residues in the tissues are rather low. Closantel is poorly metabolized. Approximately, 80% of the administered dose is excreted through the feces, of which >98% in the parent molecule form. Excretion 48 h after oral administration reaches ~45% of the administered dose, but only ~10% after intramuscular injection. Excretion half-life in the organism is 2 to 3 weeks. In dairy cows, about 1% of the administered dose is excreted unchanged through the milk. The routinely used safe-dose for the anti-helminthic action of closantel varies from 3 to 10 mg/kg depending upon the type of parasite and the animal affected. The established lethal dose limit for oral closantel in rats is 342 mg/kg, and for subcutaneous administration is 67 mg/kg of the active ingredient. Closantel intoxication has been reported in animals such as sheep, cattle, goats, and dogs.[2345] Closantel intoxication often presents with neurological and ocular features. The central nervous system, retina, and optic nerve are commonly affected. Histopathological changes noted are spongiosis in the brain white matter and spinal cord. These changes are symmetrical and affect periventricular white matter, optic radiation, brain stem, thalamic nuclei, and cerebellar peduncles. The induced histopathological changes in optic nerve following closantel overdosage include significant spongiform change, edema, and myelin vacuolization resulting in optic disc atrophy.[6] This results in edema in the intracanalicular portion of the optic nerve, which being in the osseous part gets compressed, resulting loss of myelinated axons.[6] In retina, there is destruction and apoptosis of the outer retinal layers, especially photoreceptors. The most frequent symptoms following closantel intoxication include loss of appetite, ataxia or uncoordinated movements, weakness, visual disturbances, and blindness. Other symptoms reported in sheep include depression, prostration, colic, reduced skin sensitivity, opisthotonos, nystagmus, mydriasis, loss of pupillary reflex, and blindness. Mortalities can also happen. The use of closantel in humans and milk-producing animals is strongly avoided. However, accidental ingestion of closantel leading to overdose and adverse effects in humans has been reported in literature.[78910] In humans, ocular symptoms following closantel overdosage range from sudden onset blurring of vision to total blindness. The onset of symptoms has been reported to occur from as early as 3 days to 22 years following closantel intake.[910] Depending upon the severity of damage, ocular features show optic nerve involvement ranging from blurring of disc margins and disc edema in acute stage to optic atrophy in the late stages. There is outer retinal layer thinning with spicule like hyper-pigmentation owing to the involvement of photoreceptor and retinal pigment epithelium layer. Destruction in outer retinal layers and visual pathway leads to changes in electroretinography and visual evoked potential (VEP) test. On electro-retinography, there is a reduction in both a- and b-wave amplitudes, whereas VEP shows a reduction in amplitude and delay in latency. The effects of closantel intoxication are often permanent and irreversible. There is no specific antidote for closantel. Treatment consists of supportive and symptomatic measures. Partial visual recovery with plasma exchange has been reported in a man who ingested closantel because of helminthiasis fearing.[8] To conclude, accidental closantel intake can lead to blinding visual symptoms due to outer retinal degeneration and optic atrophy.

Spontaneous Retrobulbar Haematoma.

Background. Spontaneous orbital haemorrhage is a very rare condition and vision-threatening event. It may occur due to trauma, orbital surgery/injections, orbital vascular anomalies, and a variety of systemic predisposing factors. Signs of retrobulbar hemorrhage include proptosis, ophthalmoplegia, increased intraocular pressure, loss of pupillary reflexes, and optic disc or retinal pallor. Both Computed Tomography scan and Magnetic Resonance Imaging may be performed in the diagnosis. Case Report. A 31-year-old woman was referred to our hospital with a complaint of headache and blurred vision following a strong sneeze. Ophthalmological examination revealed mild Relative Afferent Pupillary Defect in left eye. Computed Tomography revealed left hyperdense retrobulbar mass and displaced optic nerve. T1 weighted hypointense, T2 weighted hyperintense and non-enhanced round shape, sharply demarcated lesion measuring 18 × 15 × 14 × mm in diameter compatible with haematoma was detected by MRI. Surgically Caldwell-Luc procedure was performed. Histological examination confirmed haematoma. Follow-up Magnetic Resonance Imaging revealed a small reduction in the size of lesion but not complete resolution. The patient's complaint was regressed. She is now free of symptoms and is still under surveillance. To our knowledge, this is the first reported case of retrobulbar haematoma caused by sneeze.

Anisocoria and loss of pupillary reflex before CT in severe head injury

Anisocoria and loss of pupillary reflex before CT in severe head injury

Spindle coma from acute midbrain infarction

Spindle coma is an electroclinical entity in which physiologic sleep patterns, such as sleep spindles in the 9 to 14 Hz range, vertex sharp waves, and K complexes, superimposed on a background of delta and theta activity, occur synchronously in patients with altered consciousness.1 Spindle coma has been associated with structural (traumatic and nontraumatic) and nonstructural causes,2 such as cerebrovascular disease, tumor, surgery, hypoxia, seizure, drug intoxication, metabolic disturbances, and vasovagal syncope.2,3 We report three cases of spindle coma secondary to limited paramedian midbrain infarction, in which the prognosis was favorable. ### Patient 1. A 35-year-old woman presented with decreased consciousness. At the emergency room, she was comatose, with decreased and shallow respiratory effort. She had Takayasu’s disease, diagnosed 15 years previously, and was in remission. Neurologic examination showed vertical gaze ophthalmoplegia, loss of pupillary reflexes, and preserved flexor responses to pain with motor power of Medical Research Council (MRC) grade 2/5. Brain MRI revealed an isolated right paramedian midbrain infarction with thrombosis at the distal …

Fulminant hepatic failure

Abstract Analysis of the first 150 cases collected from 73 centers reporting to the Fulminant Hepatic Failure Surveillance Study showed that 80 patients had presumable viral hepatitis, of whom 62 died. Of 41 patients who had recent surgery, 36 died. In 35 patients massive liver necrosis developed less than three weeks after halothane anesthesia, and 27 (77 per cent) of these had multiple exposures to halothane. The risk from halothane is small, but this complication was present in nearly one quarter of the cases reported in our study. When the use of halothane is desired, multiple exposure should be avoided, if possible. Moreover, postoperative fever after exposure to halothane, otherwise "unexplained," is an important warning sign, and should be thoroughly investigated and taken into consideration when further exposure to this anesthetic is contemplated. The physician prescribing halothane must balance need against risk.

A Doubt About Toxic Effects of Creosote Fumes

To the Editor:— The assertion inThe Journal( 193 :745, 1965) that creosote can produce severe neurological disturbances by inhalation of its fumes is not supported by the evidence presented. Creosote was not identified as the inhalant, the concentration in the air was not measured, and there was no demonstration that creosote was present in the patient's body. Since illness resembling that which was described has not previously been attributed to creosote intoxication, it is of some importance that the conclusion of the authors be challenged. Creosote is likely to cause a skin irritation as a result of contact, and mouth and throat burns and gastroenteritis as a result of ingestion. With ingestion of large quantities, dizziness, visual blurring, loss of pupillary reflexes, kidney and liver injury are likely to result, and if the amount is very large, convulsions and death may follow. Creosote has a strong odor which most