Nursing Case Study On Cerebrovascular Accident

Mr. Smith, a businessman, has a history of hypertension. He does not take any maintenance medications and smokes three packs of cigarettes every day. During one of his meetings, he felt like he cannot speak properly. After a day, he started feeling numbness on his face, and he cannot see objects beyond his periphery. The day that he was brought to the emergency room, he cannot move his right arm and leg. He was diagnosed with ischemic stroke by the attending physician.

Contents

Description


A cerebrovascular accident (CVA), an ischemic stroke or “brain attack,” is a sudden loss of brain function resulting from a disruption of the blood supply to a part of the brain.

  • Cerebrovascular accident or stroke is the primary cerebrovascular disorder in the United States.
  • A cerebrovascular accident is a sudden loss of brain functioning resulting from a disruption of the blood supply to a part of the brain.
  • It is a functional abnormality of the central nervous system.
  • Cryptogenic strokes have no known cause, and other strokes result from causes such as illicit drug use, coagulopathies, migraine, and spontaneous dissection of the carotid or vertebral arteries.
  • The result is an interruption in the blood supply to the brain, causing temporary or permanent loss of movement, thought, memory, speech, or sensation.

Classification


Strokes can be divided into two classifications.

  • Ischemic stroke. This is the loss of function in the brain as a result of a disrupted blood supply.
  • Hemorrhagic stroke. Hemorrhagic strokes are caused by bleeding into the brain tissue, the ventricles, or the subarachnoid space.

Risk Factors


The following are the nonmodifiable and modifiable risk factors of Cerebrovascular accident:

Nonmodifiable

  • Advanced age (older than 55 years)
  • Gender (Male)
  • Race (African American)

Modifiable

  • Hypertension
  • Atrial fibrillation
  • Hyperlipidemia
  • Obesity
  • Smoking
  • Diabetes
  • Asymptomatic carotid stenosis and valvular heart disease (eg, endocarditis, prosthetic heart valves)
  • Periodontal disease

Pathophysiology


The disruption in the blood flow initiates a complex series of cellular metabolic events.

  • Decreased cerebral blood flow. The ischemic cascade begins when cerebral blood flow decreases to less than 25 mL per 100g of blood per minute.
  • Aerobic respiration. At this point, neurons are unable to maintain aerobic respiration.
  • Anaerobic respiration. The mitochondria would need to switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in pH and rendering the neurons incapable of producing sufficient quantities of ATP.
  • Loss of function. The membrane pumps that maintain electrolyte balances fail and the cells cease to function.

Statistics and Epidemiology


Stroke is a worldwide phenomenon suffered through all walks of life.

  • Morbidity: In 2005, prevalence of stroke was estimated at 2.3 million males and 3.4 million females; many of the approximately 5.7 million U.S. stroke survivors have permanent stroke-related disabilities.
  • Mortality: In 2004, stroke ranked fifth as the cause of death for those aged 45 to 64 years and third for those aged 65 years or older (National Heart, Lung and Blood Institute [NHLBI], 2007), with 150,000 deaths (American Heart Association and American Stroke Association, 2008); hemorrhagic strokes are more severe, and mortality rates are higher than ischemic strokes, with a 30-day mortality rate of 40% to 80%.
  • Cost: Estimated direct and indirect cost for 2008 was $65.5 billion (American Heart Association and American Stroke Association, 2008).
  • Stroke is the third leading cause of death after heart disease and cancer.
  • Approximately 780, 000 people experience a stroke each year in the United States.
  • Approximately 600, 000 of these are new strokes, and 180, 000 are recurrent strokes.
  • About 5.6 million noninstitutionalized stroke survivors are alive today.
  • Stroke is the leading cause of serious, long-term disability in the United States.
  • Direct and indirect costs for stroke cost $65.5 billion in 2008.
  • Strokes are usually hemorrhagic (15%) or ischemic/nonhemorrhagic (85%).
  • Ischemic strokes are categorized according to their cause: large artery thrombotic strokes (20%), small penetrating artery thrombotic strokes (25%), cardiogenic embolic strokes (20%), cryptogenic strokes (30%), and other (5%).

Causes


Strokes are caused by the following:

  • Large artery thrombosis. Large artery thromboses are caused by atherosclerotic plaques in the large blood vessels of the brain.
  • Small penetrating artery thrombosis. Small penetrating artery thrombosis affects one or more vessels and is the most common type of ischemic stroke.
  • Cardiogenic emboli.Cardiogenic emboli are associated with cardiac dysrhythmias, usually atrial fibrillation.

Clinical Manifestations


Stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion, the size of the area of inadequate perfusion, and the amount of the collateral blood flow. General signs and symptoms include numbness or weakness of face, arm, or leg (especially on one side of the body); confusion or change in mental status; trouble speaking or understanding speech; visual disturbances; loss of balance, dizziness, difficulty walking; or sudden severe headache.

General signs and symptoms include numbness or weakness of face, arm, or leg (especially on one side of the body); confusion or change in mental status; trouble speaking or understanding speech; visual disturbances; loss of balance, dizziness, difficulty walking; or sudden severe headache.

  • Numbness or weakness of the face. Without adequate perfusion, oxygen is also low, and facial tissues could not function properly without them.
  • Change in mental status. Due to decreased oxygen, the patient experiences confusion.
  • Trouble speaking or understanding speech. Cells cease to function as a result of inadequate perfusion.
  • Visual disturbances. The eyes also need enough oxygen for optimal functioning.
  • Homonymous hemianopsia. There is loss of half of the visual field.
  • Loss of peripheral vision. The patient experiences difficulty seeing at night and is unaware of objects or the borders of objects.
  • Hemiparesis. There is a weakness of the face, arm, and leg on the same side due to a lesion in the opposite hemisphere.
  • Hemiplegia. Paralysis of the face, arm, and leg on the same side due to a lesion in the opposite hemisphere.
  • Ataxia. Staggering, unsteady gait and inability to keep feet together.
  • Dysarthria. This is the difficulty in forming words.
  • Dysphagia. There is difficulty in swallowing.
  • Paresthesia. There is numbness and tingling of extremities and difficulty with proprioception.
  • Expressive aphasia. The patient is unable to form words that is understandable yet can speak in single-word responses.
  • Receptive aphasia. The patient is unable to comprehend the spoken word and can speak but may not make any sense.
  • Global aphasia. This is a combination of both expressive and receptive aphasia.

Motor Loss

  • Hemiplegia, hemiparesis
  • Flaccid paralysis and loss of or decrease in the deep tendon reflexes (initial clinical feature) followed by (after 48 hours) reappearance of deep reflexes and abnormally increased muscle tone (spasticity)

Communication Loss

  • Dysarthria (difficulty speaking)
  • Dysphasia (impaired speech) or aphasia (loss of speech)
  • Apraxia (inability to perform a previously learned action)

Perceptual Disturbances and Sensory Loss

  • Visual-perceptual dysfunctions (homonymous hemianopia [loss of half of the visual field])
  • Disturbances in visual-spatial relations (perceiving the relation of two or more objects in spatial areas), frequently seen in patients with right hemispheric damage
  • Sensory losses: slight impairment of touch or more severe with loss of proprioception; difficulty in interrupting visual, tactile, and auditory stimuli

Impaired Cognitive and Psychological Effects

  • Frontal lobe damage: Learning capacity, memory, or other higher cortical intellectual functions may be impaired. Such dysfunction may be reflected in a limited attention span, difficulties in comprehension, forgetfulness, and lack of motivation.
  • Depression, other psychological problems: emotional lability, hostility, frustration, resentment, and lack of cooperation.

Prevention


Primary prevention of stroke remains the best approach.

This is the case of a male, 50 years of age, who presented at the Palghar Hospital OPD on 20th August ’05 with tingling/numbness of the upper and lower limbs on the left side. This had begun 10 days earlier and was progressively getting worse. It began with weakness of the limbs on the left side and he was now unable to move them. An episode of severe anxiety and fear had precipitated this onset of symptoms. It had progressed further and now he had slurred speech and was laughing immoderately. He also had a strong feeling of being intoxicated ++. Along with this there had been a recurrent headache that tended to be worse in the morning, around 9-10 am.

2 months earlier he had developed hypertension. The symptoms at that point were a similar tingling and numbness on the left upper and lower limbs. This too, was precipitated by an episode of fear. He was put on anti hypertensive medication which helped and he stopped this on his own after a while.

There were no other CNS symptoms of unconsciousness, projectile vomiting, convulsions, fever or head injury.

There was no Past History of diabetes, or ischemic heart disease as possible precipitating factors.

On Examination:

Pulse: 84/min
BP: 150/100
RS: Clear
CVS: S1S2 Normal
PA: NAD
CNS: Conscious, Cooperative, Well oriented in time, space and person
Higher Functions, Cranial Nerves: Normal
No Palliloedema

MotorRightLeft
Tone: ULNormalIncreased ++
Tone : LLNormalIncreased ++
Muscle Power: ULNormalProximal Muscles: Power 1/5 Distal Muscles: Power 4/5
Muscle Power: LLNormalComplete loss of power: 0/5
Reflexes: ULNormalHypertonic ++
Reflexes: LLNormalHypertonic ++
SensoryNormalLoss of fine touch in Upper and Lower limbs

At this point in the OPD we had to decide whether this case needed to be admitted as inpatient for homeopathic management. We follow a set of criteria to make this decision for all cases, including this one. Here are the criteria that indicate mandatory in-patient admission for a homeopathic patient.

  • Close monitoring for a potentially fatal illness
  • Observation for developing complications.
  • Detailed investigation of the acute condition and risk factors.
  • Homoeopathic remedy reaction
  • Ancillary measure – physiotherapy

In this case, hospital admission was a necessity for further investigations and management to be carried out.

Investigations:

  • Hb : 15.2
  • T.L.C.: 7800 N 68 E 0 B 0 L 26 M2
  • RBS : 65.2
  • B .U. N. :9.0
  • S. CHOLESTROL : 300.2
  • S . TRIGLYCERIDES : 254
  • S. CREAT : 1.0

E.C.G. : L.V.H. Pattern

CT SCAN – BRAIN (Pictures can be viewed in the attached slide presentation)

E/o ill-defined hypodense lesion seen in the Rt high parietal lobe involving centrum semi ovale, mostly suggestive of recent non-hemorrhagic infarct in Rt MCA area.

E/o multiple lacunar infarcts in Rt internal capsule & basal ganglia.

E/o old small size infarct in Lt anterior limb of internal capsule in Lt MCA area. Periventricular white matter ischemic changes seen.

FINAL DIAGNOSIS:

LT SIDED HEMIPLEGIA, secondary to Right MCA (Middle Cerebral Artery) non-hemorrhagic infarct involving the parietal lobe of the cerebrum.

HYPERTENSION

HYPERLIPIDAEMIA

Management:

Once these preliminary medical observations are complete, we must now appraoch the case from the homeopathic standpoint for appropriate homeopathic management and care. In fact the homeopathic diagnosis is an integrated ongoing process even through the medical work being done above.

What is obvious from above, is that there already exists a chronic process going on over many months that has precipitated now as a hemiplagia (stroke). This is an acute complication of chronic disease. Our plan was to decide on the acutely indicated remedy to overcome this acute picture of symptoms, followed by the constitutional remedy. This is how we reasoned it out:

Acute remedy: There was a distinct change in the susceptibility during the acute episode that presents with new symptomatology, a clear causative factor and characteristic modalities and concomitants. These were indications for an acute remedy.

Constitutional remedy: Is expected to continue with healing of the infracted area of the brain. It is also expected to deal with the underlying causes of hypertension and hyperlipidaemia so that such episodes will not recur. In addition, the constitutional remedy must deal with the excessive tendency to be morbidly anxious and fearful over circumstances.

With this philosophical understanding of our approach, we concentrated on the acutely presenting totality which was as below:

Ailments From FRIGHT / FEAR
< ANXIETY
HEAD PAIN MORNING 10 a. m. <
STUPEFACTION, AS IF INTOXICATED, HEADACHE DURING,
LAUGHING TENDENCY, IMMODERATELY
PARALYSIS, NUMBNESS WITH,
PARALYSIS, PAINLESS
PARALYSIS ONE SIDED – LEFT

These were the rubrics chosen. Our next step was to consider which repertorization approach was appropriate to this case given the characteristic picture. Since there was characteristic sensation, modalities, concomitants, and causation, we chose the Boenninghausan’s approach for repertorization.

The remedies that came up were: Nux Moschata, Gelsemium, Opium, Rhus tox, Causticum.

Furthur discussion was required to decide on the appropriate remedy.

Along with this we also made an assessment of the Susceptiblity:

  • Susceptibility: Low Sensitivity: High
  • Pace: Slow
  • Characteristic: Few
  • Pathology: Structural – Irreversible
  • Vital organ affected

Hence the choice of posology was: Low potency with frequent repetition.

The next step was to evaluate the underlying Miasm:

  • 10 a.m. <
  • SLOW PROGRESS
  • CONFUSION
  • INTOXICATED FEELING
  • IMMODERATE LAUGHTER
  • STIFFNESS
  • HYPERLIPDAEMIA

The miasm is SYCOTIC

The final choice of remedy was Gelsemium 30C.

Follow Up:

21/08/05:

  • No headache, no giddiness,
  • Mild nuchal pain.
  • TINGLING NUMBNESS > 50%O/E:
  • BP- 140/90
  • Lt: UPPER LIMB & LOWER LIMB

    Hypertonia++
    Power – left shoulder 4/5 > ++
    left hip 3/5
    knee & ankle 0/5

Plan: Continue Gelsemium 30 QDS
23/08/05:

No TINGLING NUMBNESS.

Sensation of tightness in left upper and lower limbs > 75%

POWER: SAME

Plan: Gelsemium 200 QDS
26/08/05:

NO SUBJECTIVE COMPLAINTS

APPETITE, SLEEP NORMAL

POWER: SAME

The patient is now able to walk with support. But this support too is less that what he required earlier.

Plan: To be Discharged and follow up in OPD regularly.

Continue: Gelsemium 1M QDS.

At this stage we also considered the Chronic totality for a similimum so as to be able to appropriately begin with chronic treatment when clinically indicated. Here is the chronic picture:

The patient as a person:

  • He has 5 duaghters whom he loves very much.
  • Of all these, his 3rd daughter’s situation worried him the most. This daughter’s husband was alcoholic and had allegedly killed his first wife in a drunken rage.
  • Hence the patient remained constantly in touch with this daughter on the phone. He remained tremendously anxious about her.
  • 2 months ago when the hypertensive episode precipitated he had been unable to talk to her on the phone. Not knowing the reason for this, his got very afraid and thought that her husband had killed her. His BP went up with the intense anxiety and he began to have tingling numbness on his left side.
  • Presently due to his deteriorating health, he remains very anxious about his daughter’s future due to her alcoholic husband and his own wife’s future, as he did not have any sons.
  • He was a conscientious and a hard worker in order to support his large family of daughters.
  • In addition he is chilly, has aversion for sweets.

The Totality based on this information is:

  • ANXIOUS
  • INDUSTRIOUS
  • SYMPATHETIC
  • SENTIMENTAL
  • AVERSION SWEETS
  • CHILLY

The constitutional remedy chosen was Causticum.

Follow up:

29.8.05

On Gelsemium 1M, his gait improved further, there was no more tingling numbness, his BP was 120/80. But the weakness in his muscle power remained the same.

He was now put on Causticum 30C, 1 single powder at bedtime.

14.9.06

No intoxicated feeling

No headache

No Tingling Numbness

Power Improved:

  • Left Hip: 3/5
  • Left knee: 1/5
  • Left Shoulder: 4/5

Plan: Causticum 30C, 1 dose power daily at bedtime for 7 days.

His power continued to improve and he was normal with blood pressure well within control, anxiety considerably lessened. His lipid levels also began to reduce in time. The healing and resolution took place over a period of just a few weeks – which is remarkable in itself. That the patient chose to begin homeopathic treatment right at the outset was an important reason for such a quick resolution, before any other medication interfered with response of the vital force to an appropriate simillimum.

This is a clear example of how serious cases can be managed effectively on homeopathic treatment and management without any need for allopathic interventions, provided we have our principles of remedy choice and management clearly in place.

Click here to download the powerpoint presentation of this case.
Thank you,

Dr. Niranjan Pai, Medicine Part II

with Dr. Navin Pavaskar

Medicine Department
Dr. M.L. Dhawle Memorial Trust’s Rural Homeopathic Hospital,
Opp S.T. Workshop, Palghar – Boisar Road,
Palghar 401 404, Maharashtra, India
PH: (02525) 256932, 256933

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