Supportive management in acute stroke

1. Supportive management in
acute stroke
Dr Vaishal shah
SR Neurology
GMC, Kota

2. Introduction
• Meticulous attention to nursing and medical care is essential in
addition to thrombolysis and antiplatelet treatment in acute stroke.
• In depth understanding of type of complication that may affect stroke
patient is essential to prevent secondary brain injury.
• Focus on general medical care and supportive treatment of acute
ischemic stroke.

3. Positioning
• Unilateral middle cerebral artery occlusion – supine position is
preferable. Head up position decrease cerebral blood flow.
• No study addressing this issue in small vessel disease.
• Patient having orthopnea and on tube feeding need to be kept in
head up by 30-45 degree.
• Frequent change in position to prevent bed sore.

4. Cerebral edema
• 5 – 10%. Observed within 72-120 hours from onset.
• Most common cause of neurological deterioration in 1st week.
Increased somnolence precedes pupillary change and motor
worsening.
• Ischemic edema is initially cytotoxic and later vasogenic. Cytotoxic
edema involves predominantly gray matter, while vasogenic edema
involves predominantly white matter.

5. Cerebral edema
Risk factor for malignant cerebral edema
NIHSS of 20 or greater in dominant side, 15 or more in nondominant
side
Large vessel occlusion – terminal ICA, proximal MCA
CT – frank hypodensity within 6 hours, Infarct in 1/3 or more of MCA
territory, midline shift of 5 mm or more in 2 days
DW MRI – 80ml or more within 6 hours

6. Cerebral edema - Treatment
• Maintenance of normothermia
• Avoidance of hypercarbia, hypoxia
• Maintenance of euvolemia while avoiding hypotonic solution
• RBS between 140-180 mg/dl
• Correction of hyponatremia
• Elevation of head of bed by 15 degree.
• Intubation and mechanical ventilation when GCS<8

7. Cerebral edema - treatment
Osmotic therapy
• Hyperventilation – Maintain arterial CO2 between 30-34 mmHg
reduces ICP only for short term.
• Mannitol – 1 g/kg loading dose f/b 0.5g/kg IV 4-6 hourly with target
osmolarity between 310-320 mOsm/L
• Hypertonic saline – target sodium 150-155 mEq/L

8. Cerebral edema - treatment
osmotic therapy
• Only effective when endothelium and membrane are intact.
• Not effective within core of infarct or for cytotoxic edema. Helps
reducing extracellular edema surrounds infarct.

11. Malignant cerebral edema - treatment
• DECIMAL, DESTINY, HAMLET – craniotomy in malignant MCA infarct
• Patient younger than 60 years who deteriorate within 48 hours due
to malignant cerebral edema despite medical management should be
considered for decompressive craniotomy.
• Demonstrated decreased death and disability but no patient had
complete freedom from recovery.

12. Malignant cerebral edema - treatment
DESTINY 2 trial
• Decompressive hemicraniotomy in patients >60 years demonstrated a
significant increase in survival but most had significant disability.
• Outcome were less favourable when compared to their younger
counterpart.
• Careful selection of those with excellent prior baseline function and
few or no major comorbidities can be considered.

13. Seizure
• Intracerebral haemorrhage is associated with highest incidence of
post storoke seizure (10.6%-15.4%)
• 6.5-8.5 % ischemic stroke develop seizure ( early and late ). Incidence
is higher in cardioembolic stroke and in hemorrhagic transformation.
• SAH – around 8.5%
• TIA – 3.7%
Silverman IE, Restrepo L, Mathews GC. Poststroke seizures. Arch Neurol 2002;59:195–201.
Kalpatrick CJ, Davis SM, Tress BM, et al. Epileptic seizures in acute stroke. Arch Neurol 1990;47:157–60.

14. Seizure
• Bladdin et al. reported about 1/3rd of people with post stroke seizure
develop epilepsy.
• Cortical location
• 2/3rd – Partial seizure (Early onset). 1/3rd – GTCS (Late onset). Status
epilepticus develop in 9% of cases.
Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke. A prospective multicenter study. Arch Neurol
2000;57:1617–22.
Rumbach L, Sablot D, Berger E, et al. Status epilepticus in stroke: report on a hospital-based stroke cohort.
Neurology 2000;54:350–4.

15. Seizure
Mechanism
• Haemorrhagic stroke - Irritation caused by products of blood
metabolism.
• Ischemic stroke
Early – An increase in intracellular calcium and sodium with resultant
lower threshold for depolarisation, glutamate excitotoxicity, hypoxia,
metabolic dysfunction, global hypoperfusion – postulated theories
Late – Persistent change in neuronal excitability, gliotic scarring

16. Seizure - Treatment
• Single therapy controls seizure in 88% of cases.
• LEV, LTG > VPA
• Early post stroke seizure – Trial can be given for tapering off after 1
month treatment if no seizure activity.
• Late post stroke seizure – Generally requires long term treatment.
• No role of prophylactic treatment.

17. Blood pressure management
• Preexistant hypertension is present in 30-50% of AIS patients, acutely
elevated BP is noted on presentation with AIS in 70-80%.
• BP decline spontaneously to baseline in most over first 4-10 days after
stroke, largest drops occurs in patients with highest initial BPs.
• CBF = ( MAP – ICP )/ CVR. Cerebral autoregulation is effective
between 70-150 MAP. On higher side in chronic hypertensive
patients.

18. Blood pressure management
• AIS not eligible for thrombolytics ( onset to 72 hours )
• Hypertension should not be treated unless extreme BP increases (SBP
> 220 or DBP > 120) which may be treated to reduce BP by
approximately 15% and not more than 25% over 24 hours with
gradual reduction thereafter.
• AIS eligible for thrombolysis
• BP should be kept < 185/110 prior to tPA and below 180/105 for next
24 hours.

20. Whether to continue
pre stoke
antihypertensives??

21. Whether to continue
pre stoke
antihypertensives??
ENOS trial

22. Blood pressure management
• In ICH, both American and European guidelines recommend acute
lowering of SBP to <140 within 6 hours of onset - Driven by
INTERACT2 trial.

23. ATACH – 2 trial

25. Glucose management
• NINDS, ATLANTIS, SAINT 1 and 2 – admission hyperglycemia
considered as a continuous variable was an independent predictor of
poor neurological outcome.
• NINDS, PROACT 2 – Admission hyperglyemia predicted symptomatic
ICH after thrombolysis.
• ECASS 2 trial – 24 hours or persistent hyperglycemia (>140mg/dl) but
not baseline hyperglycemia, independent marker of poor outcome,
death and SICH in nondiabetic patients.

26. Glucose management
• Limited data on effect of hyperglycemia on spontaneous ICH. Few
small studies are showing poor outcome.
• GIST-UK trial failed to demonstrate clinical benefit of insulin induced
euglycemia ( target glucose 72-126 mg/dl ).

28. Glucose management
• AHA/ASA and ADA and AACE (association of clinical endocrinologists)
– Less intensive glycemic control of 140-180 mg/dl.
• Minimal role of OHA in inpatients – risk of acidosis, hypoglycaemia,
not suitable in critically ill patients
• DKA/ HHS/ critically ill patients/ Undergoing thrombolysis – Insulin I.V
drip is better.

29. Glucose management
• If RBS > 250mg/dl before thrombolysis – 0.1 unit/kg bolus IV regular
insulin f/b infusion.
• In HHS – if osmolarity > 320 mOsm/kg – gradual tapering to avoid
cerebral edema.
• After 48 hours, change to basal bolus.

30. Glucose management
• Insulin dosage – 0.6 * weight (50% basal, 50% to divide into 3 dose)
• Multiplier 0.3/0.4 – GFR<50 ml/min, hepatic derangement, insulin
naïve patients, well controlled sugar on diet or OHA before admission.
• Multiplier 0.7/0.8 – Obese patients, persistent hyperglycemia >250
mg/dl.

31. Cardiac abnormalities
• Serious cardiac events are common in acute stroke patients, usually
peaks 2-3 days after a stroke.
• Patients with ischemic and haemorrhagic stroke have been shown at
autopsy to have subendocardial haemorrhages and focal regions of
necrosis of cardiac muscle.
• ECG changes consistent with ischemia, elevated CPK and troponin,
cardiac arrythmias are found in stroke patients without previous
cardiac illness.

32. Cardiac abnormalities
• Three ways of cardiac involvement in stroke
1. Direct involvement of critical structure – Insula, hypothalamus,
brainstem nuclei that make up the central autonomic network
2. Mass effect with compression of hypothalamus or brainstem or
both that activates autonomic pathways
3. Acute brain lesion and its stress effects stimulate the hypothalamic
pituitary axis triggering release of corticosteroid and catecholamine.

33. Cardiac abnormalities
• Patients with SAH and vertebrobasilar territory ischemia sometimes
develop acute pulmonary edema.
• Weir attributed sudden severe increase in ICP , which in turn causing
massive autonomic stimulation.
• Old patients with cerebral hemispheric infarction have greatest risk
for cardiac arrythmias.

34. Cardiac abnormalities
• Careful attention to CVS with regular examination, monitor vitals,
regular ECGs.
• Beta blockers – propranolol and other for arrythmias. Not proven yet
but effective in animal studies.
• Cardiologist advice for management arrythmias.

35. Role of hypothermia

36. Role of neuroprotective agents

37. Venous thromboembolism
• Incidence of pulmonary embolism in first few months – 1-3%
• Early death after stroke due to pulmonary embolism – 13-25%
• Fatal embolism are seen most commonly encountered in weeks 2 to 4
• Peak incidence of DVT between 2-7 days

38. Venous thromboembolism
Risk factor for DVT
• Severity of impaired mobility
• Dehydration
• Advanced age
• Malignancy
• Prior history of DVT
• Clotting disorders

44. Josephine F et al. Prevention and management of poststroke complication, Continuum (Minneap Minn) 2017;23(1):93–110.

45. Venous thromboembolism - Prevention
• Physical therapy is started at the bedside - flex and extend the knees
and ankles throughout the day.

46. Infection
• Fever after stroke – Prompt evaluation for common sources including
pneumonia, UTI
• Most common cause of fever in first 48 hours after acute stroke is
pneumonia, which is attributed to aspiration in 60% of cases.
• Aspiration – decreased alertness, dysphagia and other neurological
deficits like apraxia, agnosia, depression.

47. Infection - Aspiration
• In recumbent position – atelectasis and poor mobilisation of
secretions.
• Coughing and deep breathing may not be performed.
• Decreased chest movement, decreased respiratory drive and function
of interstitial muscles often abnormal on hemiplegic side. Kaldor and
berlin noted pneumonia on hemiplegic side.
Kaldor A, Berlin I: Pneumonia, stroke, and laterality. Lancet 1981;1:843.

48. Infection – Aspiration prevention
• Prevention of aspiration pneumonia begins with proper identification
of patients with dysphagia.
• Dysphagia – 29-45% in acute stage of stroke, 47% on a rehabilitation
unit 2-3 weeks poststroke, 17% at 2-4 months follow up.
• Clinical judgement – palpation of hyoid bone for adequate rising while
swallowing, wet voice, spontaneous cough after swallowing, checking
oral cavity for pocketing of food

49. Infection – Aspiration prevention

50. Infection – Aspiration prevention
• Standard practice is to change consistency of food. Not proven.
• Manouvres like chin tuck, head turn, Mendelsohn’s manoeuvre.
Efficacy remains controversial.
• Regular chlorhexidine mouth wash.
• Early mobilisation and good pulmonary care

51. Infection – Aspiration prevention
• Nausea should be addressed and treated to prevent vomiting.
• For intubated patients. Ventilation in semirecumbent position,
appropriate airway positioning, suctioning of secretions, daily
assessment of potential extubation.
• Nasogastric feeding and PEG feeding – till now no study has proven its
efficacy in non dysphagic patients in preventing aspiration but it
improves nutritional status.

54. Infection - prevention
Points to consider for tube feeding
Head end elevation of at least 30 . Keep same for an hour afterward.
Tube fed patient is able to communicate – vigilant about sign of slow
gastric emptying like nausea, fullness, abdominal pain, cramping
Patient not able to communicate – abdominal distention and large
gastric residua are indicator of slow gastric emptying.
Monitor tube location every 4 hours. Displacement of tube into
oesophagus also increases risk of aspiration.

55. Infection - prevention
Points to consider for tube feeding (cont.)
To check gastric residual volume (GRV) every 4 hourly. Feeding should
be interrupted if GRV is above 200-250 ml. Prokinetic can be tried.
Continuous feeding is found better than bolus feeding in some small
studies but no recommendation can be made.
ET cuff pressure should be >20 cm H2O. Hypopharyngeal suctioning
should be performed before cuff is deflated.
Smallest effective dose of sedation to prevent cough reflex.

59. Infection
• UTI – seen in 11-15% of stroke patients. Often seen during first 5
days, but can occur up to 3 months poststroke.
• 2 mechanism
1. Indwelling catheter – allows introduction and growth of bacteria.
Condom catheter for men and intermittent catheterisation using
strict sterile technique for females.
2. Functioning of bladder and external sphincter can be compromised
by stroke.

60. Infection
• Tsuchida et al.
Frontal and internal capsule lesions – hyperactive bladder with
uninhibited sphincter relaxation – frequency/incontinence
Putaminal lesions – hyperactive bladder with normal sphincter
• Frequent voiding during day and night to train bladder. USG abdomen
to look for post voidal residue and to rule out BPH. Frequent urinary
examinationto r/o UTI.

61. Nutrition
• Malnutrition contributes to diminished immune function, cardiac and
gastrointestinal dysfunction, abnormal bone metabolism.
• Malnutrition – a factor in formation and repair of decubitus ulcer.
• A study showed that improvement of neurocognitive deficits
correlated positively with dietary protein intake and negatively with
the carbohydrate/protein intake ratio.

62. Nutrition
• An individualized energy- and protein-supplementation diet during
hospital stay also improved health-related quality of life and grip
strength after 3 months
• Currently, no single formula to calculate nutrition requirements but
total energy expenditure (TEE) remains low in acute stroke.

63. Nutrition
• Daily protein intake >1 g/kg in order to achieve a
carbohydrate/protein ratio <2.5
• Energy intake ≥25 kcal/kg in non-obese subjects to maintain body
weight and <25 kcal/kg in obese subjects to maintain a
carbohydrate/protein ratio <2.5.
• Dehydration should be avoided. Increase the risk of DVT and worsen
neurological injury. Overnight IV fluid administration is advised. NS at
a rate of 1-2ml/kg/hour in whom normal oral fluid intake is not
feasible.

64. Hyponatremia
• Approx 15% develop hyponatremia.
• SIADH and CSWS
• Damage to anterior hypothalamus, effects on ADH secretion related
to recumbency, resetting of osmoreceptors, damage to a more
widespread vasopressin neuronal system, increased release of ADH,
secondary stroke related elevation in serum catecholamine and
cortisol
Joynt RJ, Feibel JH, Sladek CM: Antidiuretic hormone levels in stroke patients. Ann Neurol 1981;9:182–184.

67. Hyponatremia
• SIADH – fluid restriction, 3% saline, furosemide, tolvaptan
• CSWS – Normal saline, 3% saline, fludrocortisone.

68. Gastrointestinal issues
Constipation
• Seen in 16% of stroke patients.
• Immobility, dehydration, hypokalemia, diet change are culprit.
• Treatment - Early mobilisation, hydration, avoidance of anticholinergic
drugs, use of stool softeners, bulk forming agents, laxatives.

69. Pressure sore

70. Pressure sore
Prevention

71. Pressure sore treatment by NPUAP

72. THANK YOU

73. References
• 2018 AHA guidelines for acute ischemic stroke
• Textbook of “Prevention and treatment of ischemic stroke”
• Textbook of “Bradley’s neurology in clinical practice 7th edition”
• Textbook of “Caplan’s stoke – A clinical approach 5th edition”
• Josephine F et al. Prevention and management of poststroke
complication, Continuum (Minneap Minn) 2017;23(1):93–110.
• Textbook of “Stroke recovery and rehabilitation 2nd edition”
• www.uptodate.com
• P K Myint et al. Post-stroke seizure and post-stroke epilepsy, Postgrad
Med J 2006;82:568–572.