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Acute liver failure (ALF) is a life-threatening condition where the liver quickly loses its function. It usually occurs in people without prior liver disease and requires immediate medical care. How it affects the body The liver sustains severe damage and cannot perform essential functions. This can lead to confusion, bleeding problems, and other serious complications. Common causes Acetaminophen overdose, often accidental. Viral hepatitis, such as Hepatitis A or E. Toxins from herbal products, mushrooms, or chemicals. Autoimmune hepatitis, where the immune system attacks the liver. Wilson’s disease, a genetic disorder causing copper buildup. Key symptoms Jaundice: Yellowing of the skin and eyes. Hepatic encephalopathy: Confusion or altered mental state. Bleeding and bruising due to impaired clotting. Nausea, abdominal discomfort, and loss of appetite. Fatigue and general weakness.

Acute kidney injury (AKI) occurs when the kidneys suddenly lose their ability to filter waste products from the blood. As wastes and fluids build up, the body’s chemical balance can become dangerously disrupted. AKI was previously called acute kidney failure and is most common in hospitalized patients, especially those in intensive care. AKI can range from mild to severe. In serious or untreated cases, it can be life-threatening. However, when identified early and managed properly, AKI is often reversible, and many people—especially those who were previously healthy—can recover normal or near-normal kidney function. Symptoms AKI may cause: Reduced urine output Fluid buildup leading to swelling of legs, ankles or feet, and shortness of breath Fatigue and weakness Confusion or mental fog Nausea or loss of appetite Pain in the abdomen or side below the ribs Irregular heartbeat Itching Chest pain or pressure Seizures or coma in severe cases Sometimes AKI causes no noticeable symptoms and is discovered through routine blood tests. When to see a doctor Seek medical attention immediately if you have symptoms suggestive of acute kidney injury. Early diagnosis and treatment are critical to prevent serious complications.

Lacunar Syndromes – Clear Clinical Overview Lacunar syndromes are a group of distinct neurological presentations caused by small deep infarcts (lacunes) in the brain. These infarcts result from occlusion of small penetrating arteries, most commonly due to chronic hypertension, but also diabetes and smoking. Unlike large strokes, lacunar strokes do not involve the cerebral cortex, which explains their characteristic pattern of symptoms. The Five Classical Lacunar Syndromes 1. Pure Motor Stroke (Pure Motor Hemiparesis) Most common lacunar syndrome Weakness or paralysis of the face, arm, and leg on one side No sensory loss Common lesion sites: Posterior limb of the internal capsule Basis pontis 2. Pure Sensory Stroke Numbness, tingling, or altered sensation on one side of the body No motor weakness Typically involves the thalamus (especially the ventral posterolateral nucleus) 3. Ataxic Hemiparesis Combination of: Ipsilateral weakness Poor coordination (ataxia), especially affecting gait Often appears as “clumsy walking” Common lesion sites: Pons Internal capsule Corona radiata 4. Dysarthria–Clumsy Hand Syndrome Slurred speech (dysarthria) Clumsiness and poor fine motor control of the hand Facial weakness may be present Lesions usually located in: Pons Internal capsule 5. Mixed Sensorimotor Stroke Motor weakness and sensory loss on the same side of the body Often due to lesions involving both: Thalamus (sensory) Internal capsule (motor) Causes & Pathophysiology Lacunar strokes result from disease of small penetrating arteries: 🔹 Main mechanisms Occlusion of a single small artery Lipohyalinosis Vessel wall thickening and degeneration from chronic hypertension Microatheroma Small atherosclerotic plaque within the penetrating artery 🔹 Resulting lesion Lacune: A small, fluid-filled cavity in brain tissue Size: 3–15 mm Common Brain Locations Involved Internal capsule Thalamus Pons Basal ganglia Corona radiata These are deep brain structures, which explains the symptom pattern. Diagnosis & Key Clinical Characteristics Diagnosis Clinical syndrome recognition is essential MRI (especially DWI) confirms diagnosis by showing a small deep infarct Key distinguishing features ✅ Deficits confined to motor and/or sensory pathways ❌ No cortical signs, such as: Aphasia Neglect Visual field loss Seizures This absence of cortical features helps differentiate lacunar syndromes from larger territorial strokes. Clinical Importance Lacunar strokes often have better short-term survival, but: Recurrent lacunes can lead to vascular dementia Associated with chronic small vessel disease Strongly linked to long-standing uncontrolled hypertension