![]() N –acetyl cysteine (NAC) and 3% NS were started as per protocol. Arterial blood gases, blood sugar and electrolyte were monitored and managed. Core temperature was maintained at 35-36 0C. The patient was nursed in slight head up position with no physical stimulation. Haemodynamics were maintained on high dose nor adrenaline and low dose vasopressin infusions. Invasive haemodynamic monitoring helped guided fluid management. Trechea was electively intubated in view of encephalopathy with etomidate, fentanyl and rocuronium and mechanical ventilation instituted targrting an end tidal CO 2 of 30-35 mmhg. The patient was managed according to institute protocol for ALF. Other lab parameters were as follow haemoglobin 9 gm% TLC: 10,400 mm3 platelet count 1.24 lacs mm3 bilirubin 42.2 mg% AST: 453 IU/ml ALT:719 IU/ml INR:5.43 sodium: 134 meq/l potassium: 3.52 meq/L serum creatinine 0.9 mg%. A provisional diagnosis of ALF with unknown etiology was made. On examination patient was in hepatic encephalopathy grade 4 with bilateral equal mid dilated pupil sluggish reacting to light. In this situation patient was reffered to our institute. Patient was apparently normal 20 days back then she developed fever which is acute in onset not associated with chills and rigor but associated with nausea and vomiting and jaundice which was insidious in onset, gradually progressive in nature and not associated with pruritis or clay coloured stool for which she was admiited in local hospital there she developed altered sensorium which is acute in onset, started as confusion and progressed to agitation followed by non responsive to verbal stimuli. This is known as idiopathic Horner syndrome.A 42 old years female patient with no other co morbidities. In some cases, the cause of Horner syndrome cannot be identified. Tumor of the hormonal and nervous systems (neuroblastoma).Injury to the neck or shoulders during delivery.The most common causes of Horner syndrome in children include: Cluster headaches, a disorder that results in cyclical patterns of severe headaches.Tumor or infection near the base of the skull.Damage to the jugular vein along the side of the neck.Damage to the carotid artery along the side of the neck.Nerve damage in this region may be associated with the following: This neuron path extends along the side of the neck and leads to facial skin and muscles of the iris and eyelids. Damage to the main blood vessel leading from the heart (aorta).Tumor of the myelin sheath (schwannoma).Causes related to nerve damage in this region may include: This neuron path extends from the spinal column, across the upper part of the chest and into the side of the neck. Cyst in the spinal column (syringomyelia).Diseases that cause the loss of the protective sheath on neurons (myelin).Problems in this region that can disrupt nerve function related to Horner syndrome include: This neuron pathway leads from the hypothalamus at the base of the brain, passes through the brainstem and extends into the upper portion of the spinal cord. The nerve pathway affected by Horner syndrome is divided into three groups of nerve cells (neurons). The sympathetic nervous system regulates heart rate, pupil size, perspiration, blood pressure and other functions that enable you to respond quickly to changes in your environment. Horner syndrome is caused by damage to a certain pathway in the sympathetic nervous system. Muscle weakness or lack of muscle control.Get emergency care if signs or symptoms associated with Horner syndrome appear suddenly, appear after a traumatic injury, or are accompanied by other signs or symptoms, such as: It is important to get a prompt and accurate diagnosis. ![]() Change in color on the affected side of the face that would typically appear from heat, physical exertion or emotional reactionsĪ number of factors, some more serious than others, can cause Horner syndrome.Lighter iris color in the affected eye of a child under the age of 1.ChildrenĪdditional signs and symptoms in children with Horner syndrome may include: Signs and symptoms, particularly ptosis and anhidrosis, may be subtle and difficult to detect. Little or no sweating (anhidrosis) on the affected side of the face.Slight elevation of the lower lid, sometimes called upside-down ptosis.Little or delayed opening (dilation) of the affected pupil in dim light.A notable difference in pupil size between the two eyes (anisocoria).Horner syndrome usually affects only one side of the face.
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