Vinolia Diag- acute ishmic stroke Known for left mca watershed infract Recurrent crebrovascular accident Acute ischaemia stroke Know for Acute cva lt mca infract Rt ataxic hemiparesis, dysarthria,umn palsy B/l icad mca stenosis 98 year female known case left mca water shed infracton , treatment received but not on medications Presented drowsiness, angio,mri Brain Acute stroke left aca ,mca internal boderzone infract , thrombotic occlusion of left mca territory Patient conscious Ecg bradycardia around 60/min No history of Cardiac , seizures tongue bite ,fever vomit , urine Just less interactive. More sleeping decline response Amidon 3ml inj Optineuron 3ml inj Magnet forte 3ml inj Adana 1gm Metalorb25mg 10cc nipro 5cc nipro Apixapil 2.5mg Ns 100ml fres8nus kabi inj 2cc bd emerald syringe with needle Cannula Pantocid40mg inj Candid powder Plasmosal 1000ml inj Strocit 500mg Clopilet75mg Ecosprin 75mg Arousal 40mg Cremaffin pink 170ml syrup Corcell tab Oki- d3 60kiu capsules Wbc 13000 to 11000 progress Mch 32.7 Mchc 35.2 Neutrophil lymphocytes ratio 6.0% C reactive protein 88.3 to 32.3 Mild concentric lvh

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"intracranial atherosclerosis" AND "stroke" AND "management"

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"acute ischemic stroke" AND "elderly" AND "antiplatelet"

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Clinical Analysis: Vinolia - 98F, Recurrent Ischemic Stroke with B/L ICAD-MCA Stenosis


Diagnosis Summary

Primary: Acute ischemic stroke - Left ACA-MCA internal borderzone (watershed) infarct, with thrombotic occlusion of left MCA territory
Background:
  • Recurrent CVA - known Left MCA watershed infarction (prior event)
  • Bilateral intracranial atherosclerotic disease (ICAD), MCA stenosis
  • Right ataxic hemiparesis, dysarthria, UMN signs (lacunar-type + cortical involvement)
  • Mild concentric LVH (cardiac)
  • Age 98, not on maintenance medications prior to this admission

Understanding the Infarct Pattern

Watershed (Borderzone) Infarction in the ACA-MCA territory is the classic consequence of:
  • Proximal arterial stenosis (here, MCA stenosis) causing low distal perfusion pressure
  • The cortical region at the border between two arterial territories is the most vulnerable to ischemia when perfusion drops
As described in Neuroanatomy through Clinical Cases 3rd Edition:
"Pressure in a patient with carotid stenosis can cause an ACA-MCA watershed infarct, since the MCA and ACA are both fed by the carotid. Watershed infarcts can produce proximal arm and leg weakness ('man in the barrel' syndrome) because the regions of homunculus involved often include the trunk and proximal limbs."
In this case, the culprit is bilateral MCA ICAD rather than carotid stenosis, but the hemodynamic mechanism is the same.
Thrombotic occlusion of the left MCA adds an embolic/thromboembolic component on top of the pre-existing stenosis, producing the acute deterioration.

Clinically Notable Features

FindingInterpretation
Right ataxic hemiparesis + dysarthriaLacunar syndrome (paramedian pontine or internal capsule) - a recognized presentation in ICAD
UMN palsy (right side)Left hemisphere cortical/subcortical involvement consistent with MCA territory
Drowsiness / decreased responsivenessLarge territory involvement; raised ICP possible; possible metabolic component
ECG: bradycardia ~60 bpmSinus bradycardia - may be vasovagal, medication effect (metoprolol/Metalorb), or rarely Cushing response if ICP rising
WBC 13,000 → 11,000 (trending down)Reactive leukocytosis, improving - likely stress response or aspiration pneumonia treatment
CRP 88.3 → 32.3 (improving)Significant systemic inflammation now resolving - monitor for infection (aspiration pneumonia is a top risk in stroke)
MCH 32.7, MCHC 35.2Normal red cell indices - no obvious hemoglobin defect
Neutrophil:Lymphocyte ratio 6.0Mildly elevated - consistent with acute inflammatory/stress state
Mild concentric LVHChronic hypertensive end-organ damage; no acute cardiac source documented
Ataxic hemiparesis + dysarthria in this context is characteristic of a lacunar infarct, typically in the posterior limb of the internal capsule or pons. Localization in Clinical Neurology 8e confirms: "Most patients show slight hemiparesis with ataxia and dysarthria, ataxic hemiparesis, or dysarthria-clumsy hand syndrome" with paramedian pontine or capsular pathology.

Medication Review

Current Prescriptions - Analysis

DrugClassIndication in This Case
Ecosprin 75 mg (aspirin)AntiplateletAntiplatelet - correct for ischemic stroke secondary prevention
Clopilet 75 mg (clopidogrel)AntiplateletDual antiplatelet therapy (DAPT) - appropriate in acute/recurrent ischemic stroke with ICAD
Apixaban 2.5 mgDOAC (Factor Xa inhibitor)This needs careful scrutiny - see below
Strocit 500 mg (citicoline)NeuroprotectiveUsed for neuroprotection/neuronal membrane repair in stroke - common practice in India
Metalorb 25 mg (metoprolol succinate)Beta-blockerRate/BP control - watch in context of bradycardia (HR ~60) - consider dose review
Arousal 40 mgLikely atorvastatinStatin therapy - correct for ICAD and stroke secondary prevention
Pantocid 40 mgPPI (pantoprazole)GI protection, especially with dual antiplatelet
Adana 1 gmLikely tranexamic acid or aminocaproic acid - confirmIf antifibrinolytic, use with caution alongside antiplatelets
Amidon 3 ml (injection)Likely amikacinAntibiotic - for pneumonia/UTI risk management
OptineuronB-complex (thiamine, B6, B12)Neurotropic vitamins
Magnet forteMagnesium supplementNeuromuscular support
Plasmosal 1000 mlPlasma-lyte/balanced crystalloidIV fluid maintenance
NS 100 mlNormal salineIV access/flush
Cremaffin pinkLaxativePrevent constipation (immobility risk)
Corcell tabLikely CoQ10 or cardiac supplementCardioprotection
Oki-D3 60K IUCholecalciferolVitamin D supplementation
Candid powderClotrimazole (antifungal)Skin/perineal care (pressure areas)

Key Clinical Concerns

1. Triple Antithrombotic Therapy (CRITICAL)

Patient is on aspirin + clopidogrel + apixaban (2.5 mg) simultaneously. This is triple antithrombotic therapy - carrying a significantly elevated bleeding risk (intracranial hemorrhage, GI bleed) in a 98-year-old.
Apixaban 2.5 mg is the reduced dose used in:
  • Elderly patients (age ≥80) with AF + low body weight or renal impairment
  • There is no documented AF or valvular heart disease in this case summary
Evidence note: Per Goldman-Cecil Medicine:
"Urgent anticoagulation to prevent recurrent stroke, to prevent worsening, or to improve functional outcome of patients with acute ischemic stroke is NOT recommended."
DAPT (aspirin + clopidogrel) is evidence-based for high-risk TIA or minor stroke for 21 days, then step down to monotherapy. Adding apixaban without a clear indication (AF, cardiac thrombus, hypercoagulable state) is outside guideline recommendations and significantly raises hemorrhagic transformation risk - especially with bilateral MCA thrombotic occlusion.
Action point: Confirm indication for apixaban. If no AF on ECG/Holter, consider discontinuing or substituting.

2. Bradycardia + Metoprolol

HR ~60 bpm with metoprolol ongoing. In acute ischemic stroke, relative hypotension and bradycardia can worsen ischemia in borderzone territories (hemodynamic mechanism).
  • Do not aggressively lower BP unless >220/120 mmHg (no thrombolysis given)
  • Review if metoprolol dose is contributing to bradycardia

3. Bilateral ICAD - MCA Stenosis Management

Per Bradley and Daroff's Neurology in Clinical Practice:
  • The WASID trial showed 23% annual recurrent stroke rate in patients with >70% intracranial stenosis despite medical therapy
  • The SAMMPRIS trial showed intensive medical management (aspirin + clopidogrel + statin + BP/lifestyle control) was superior to Wingspan stenting for ICAD
  • Wingspan stent FDA criteria require age 22-80 years - this patient at 98 is outside surgical/endovascular candidacy
Optimal medical management for ICAD:
  • DAPT (aspirin + clopidogrel) - already prescribed
  • High-intensity statin (atorvastatin 40-80 mg) - confirm Arousal dosing
  • Strict BP control (target <140/90 at 1 week; avoid acute drops acutely)
  • Risk factor modification

4. Decreased Responsiveness / "More Sleeping"

Differential in this patient:
  • Large hemispheric infarct with mass effect
  • Metabolic derangement (check glucose, sodium, renal function)
  • Post-ictal state (though no documented seizure)
  • Medication sedation
  • Aspiration pneumonia / sepsis (CRP was 88 - now improving)
  • Herniation if infarct is swelling (watch pupils, GCS closely)
Ensure: Head of bed elevated 30°, aspiration precautions, swallow assessment before any oral intake, glycemic monitoring.

5. Age 98 - Goals of Care

This patient has now had at minimum two significant hemispheric strokes. At 98 years with bilateral MCA ICAD and recurrent thrombotic occlusion:
  • Aggressive interventions (thrombolysis, thrombectomy, stenting) are largely contraindicated or unlikely to improve outcomes
  • Palliative and rehabilitative goals should be discussed with family
  • Focus: comfort, aspiration prevention, skin care, bowel/bladder management, physiotherapy

Recommended Immediate Actions

  1. 12-lead ECG + Holter monitoring - rule out paroxysmal AF (to justify apixaban or remove it)
  2. Review triple antithrombotic - if no AF, discontinue apixaban; continue DAPT for 21 days then step to monotherapy (clopidogrel preferred in ICAD)
  3. Neurology consult - assess degree of consciousness decline, rule out herniation
  4. Swallow assessment - nil per mouth until assessed (aspiration pneumonia risk with CRP elevation)
  5. Glucose, BMP, LFTs - metabolic causes of drowsiness
  6. Metoprolol dose review - bradycardia at 60 bpm is borderline; avoid drops in cerebral perfusion pressure
  7. CT head - if not recently done, assess for hemorrhagic transformation (before continuing antithrombotics)
  8. Statin optimization - ensure atorvastatin 40-80 mg (high-intensity) is given
  9. Pressure area care - Candid powder suggests awareness, continue nursing care
  10. Family/carer counseling regarding prognosis and goals of care

Summary of Infarct Mechanism

Bilateral MCA ICAD (>70% stenosis)
        ↓
Reduced distal perfusion pressure
        ↓
ACA-MCA internal borderzone = most vulnerable zone
        ↓
Chronic watershed infarcts (prior history)
        ↓
Acute thrombotic occlusion of left MCA (this episode)
        ↓
Acute superimposed territorial + watershed infarction
        ↓
Right hemiparesis (UMN) + ataxia + dysarthria + decreased consciousness

Sources: Goldman-Cecil Medicine (p. stroke chapter), Bradley and Daroff's Neurology in Clinical Practice (ICAD chapter), Neuroanatomy through Clinical Cases 3e (watershed infarct section), Localization in Clinical Neurology 8e (ataxic hemiparesis)
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