Emergency Management in Vascular Conditions

1. REVIEW OF LITERATURE
1

2. Emergency Disorders And
Management in Vascular
Diseases
Dr Devanshi Jobanputra
Final Year PG – Department of CVRS
2

3. CONTENTS
Introduction
Types of Vascular Diseases and Categorizing Them
Risk Factors/Causes
Pathophysiology
Clinical Manifestations
Medical Management
Physiotherapy Management
Evidences
References
3

4. Vascular Diseases
• Diseases that affect the blood vessels , which causes
a disturbance in the carbon dioxide and oxygen
balance.
• Due to the disturbance the flow of blood in the
vessels is blocked.
• Causes :
• High cholesterol.
• High blood pressure.
• Smoking.
• Diabetes.
• Hereditary.
• Injury.
• Blood clots. 4

5. Types of Vascular Diseases
• Coronary Artery Disease- Myocardial Infarction
• Shock
• Acute Pulmonary Edema
• Acute Respiratory Distress Syndrome
• Respiratory Failure
• Pulmonary Embolism
• Stroke
• Subarachnoid Haemorrhage
• Increased Intracranial Pressure and Head Trauma
• Hypoxic Ischaemic Encephalopathy
5

6. Categorizing Emergency Vascular Disorders
CARDIAC PULMONARY NEUROLOGICAL
Coronary Artery
Disease (CAD)
Acute Pulmonary Edema Stroke
Myocardial
Infarction (MI)
Acute Respiratory Distress
Syndrome (ARDS)
Increased Intracranial Pressure (ICP)
and Head Trauma
Shock Respiratory Failure (RF) Hypoxic Ischaemic Encephalopathy
(HIE)
Pulmonary Embolism (PE)
6

7. Early Warning For Referral Of ‘At Risk’ Patients
To The Critical Care Team
7

8. Cardiovascular Collapse And Sudden Death
• Unexpected cardiovascular collapse and sudden death most often caused due to
patients with acute or chronic atherosclerotic coronary artery disease.
• Other common etiologies are :
Structural Causes Functional Contributing Causes
Coronary Heart Disease Transient Ischaemia
Myocardial Hypertrophy Low Cardiac Output : a) Heart Failure
b) Shock
Inflammatory (myocarditis) Electrolyte Imbalance- Hypokalaemia
Valvular Heart Diseases Neurologic Disturbances- CNS Injury
8

9. Coronary Artery Disease
• Narrowing of the coronary arteries that prevents
adequate blood supply to the heart muscle is
called coronary artery disease. Usually caused
by atherosclerosis, it may progress to the point
where the heart muscle is damaged due to lack
of blood supply. Such damage may result in
infarction, arrhythmias, and heart failure.
• Coronary atherosclerosis is the abnormal
accumulation of lipid or fatty substances or fatty
atheroma (plaque) in the lumen of coronary
artery.
9

10. Risk Factors
10

11. Pathophysiology
11

12. Signs & Symptoms
12

13. Medical Management
• Nitrates
• Beta adrenergic blockers(atenolol)
• Calcium channel blockers(nifedipine)
• Ace inhibitors(captopril)
• Statins
• Surgical intervention
1. Stents
2. Coronary Artery Bypass Grafting (CABG)
3. PTCA
13

14. • Lifestyle changes that may
be useful in coronary
disease include:
• Weight control
• Smoking cessation
• Exercise
• Healthy diet
14

15. Myocardial Infarction
• Necrosis occurring as a result of a
critical imbalance between
coronary blood supply and
myocardial demand.
• It is usually due to the formation of
an occlusive thrombus at the site of
rupture of an atheromatous plaque
in coronary artery.
15

16. Signs And Symptoms Of Myocardial Infarction
Symptoms Signs
Chest Pain Tachycardia/Bradycar
dia
Breathlessness Raised JVP
Vomiting Pallor
Fatigue Sweating
Syncope Systolic Murmur –
Mitral Regurgitation
16

17. Initial Management
• Attach a cardiac monitor.
• Secure an intravenous line.
• Administer oxygen.
• Administer sublingual nitrate.
• If no relief, give IV morphine 3-5 mg.
• Give Asprin 150 mg to be chewed.
• Give clopidogrel 300 mg orally.
17

18. Management Of A Patient With Cardiac Arrest
• Basic Life Support must commence immediately.
• BLS Basic Life Support (BLS) is a specific level of pre-hospital medical care
provided by trained health care providers responders in the absence of advanced
medical care.
• BLS consists of cardiopulmonary resuscitation (CPR) or emergency cardiac
care (ECC) that is medical care which is used for patients with life threatening
illness or injury until the patient can be given full medical care.
• Sequences of procedure performed to restore the circulation after a sudden
pulmonary or cardiac arrest.
• CPR is a combination of rescue breathing and chest compression delivered to
victims in cardiac arrest.
18

19. • Performing the method of CPR
with good quality of chest
compression with minimal
interruption.
• Start CPR immediately.
• Brain damage starts in 4 to 6
minutes.
• Brain damage is certain after 10
minutes without CPR.
• Effective CPR provides ¼ to 1/3
normal blood flow.
19

20. • Push hard, push fast.
• Compress at a rate of 100 compressions per minute.
• Allow full chest recoil after each compression.
• Minimize interruption in chest compression.
• Try to keep in less than 10 seconds.
20

21. 21

22. Points To Remember While Administering CPR
• Position yourself at the victims side so that you are ready to open the airway
and giving breaths.
• When doing head tilt chin lift do not press deeply into the soft tissue under the
chin because this might obstruct the airway.
• Do not give breaths too quickly or with too much force, air is likely to enter the
stomach rather than the lungs which can cause gastric inflation.
• Rescuer should use a universal compression-ventilation of 30 is to 2 breaths
when giving CPR to victims of all ages except for the neonates.
• Two rescuer should use a compression-ventilation ration of 15 is to 2 breaths
when giving CPR to children and infants.
22

23. • The correct rate for giving compression is 100 compressions a minute.
• Rescuers should try to minimize interruptions to less than 10 seconds.
• Continue resuscitation until qualified help arrives and takes over, the victim
starts breathing normally and rescuer becomes exhausted.
• The correct compression-ventilation ration for and adult is 30 compression
and 2 breaths.
• Minimize interruption in chest compressions, try to keep interruptions to 10
seconds or less.
23

24. Shock
• Shock is defined by the presence of
multisystem end-organ hypoperfusion.
• Condition leading to cellular injury and
dysfunction.
• Cardinal Features Of Shock
Hypotension with a SBP <90mmHg
Tachycardia >100bpm
Cold skin and extremities
Cheyne-Stokes Breathing
Urine Output <30mL/hour
24

25. Classification And Causes Of Shock
Hypovolaemic Shock: Haemorrhage, Severe Vomiting and
Diarrhoea , Plasma Loss in Burns.
Cardiogenic Shock: Acute myocardial infarction, Acute
Aortic Regurgitation, Acute Mitral Regurgitation, Rupture
of Interventricular Septum, Myocarditis, Excessive
Diuretic Therapy
Septic Shock: Gram positive and Gram negative Bacterial
Infections.
Anaphylactic Shock: Drugs, Insect Stings.
Neurogenic Shock: Severe Head Injury.
25

26. Clinical
Manifestations,
Diagnosing and
Management of
Shock
26

27. Management
• Patient Monitoring:
1. Pulse Rate, Blood Pressure, Respiratory Rate.
2. ECG: Monitoring for Rate and Rhythm.
3. ABG and pH for corrections of acidosis and Hypoxia.
4. Urinary Catheterization to Monitor Urinary Output.
• General Measures :
1. Care of skin, airway, bowel and bladder and nutrition.
2. Hypovolemia is corrected usually by blood transfusion.
3. Correction of hypoxia with O2 by face mask or nasal prongs , if necessary by
intubation and mechanical ventilation.
27

28. Physiotherapy Management
1.Lay the Person Down, if Possible: Elevate the person's feet about 12 inches.
Do not raise the person's head.
2.Turn the person on side if they are vomiting or bleeding from the mouth.
3. If the patient is breathless, the patient is taught pursed lip breathing.
4.Begin CPR, if Necessary: If the person is not breathing start CPR and continue
until help arrives or the person wakes up.
5.Keep the Person Warm and Comfortable: Loosen restrictive clothing. Cover
with a coat or blanket.
28

29. Pulmonary Edema
• Pulmonary oedema is defined as an abnormal
accumulation of fluid in the extravascular
compartments of the lung parenchyma. This
process leads to diminished gas exchange at
the alveolar level, progressing to potentially
causing respiratory failure.
• Its main pathophysiologic mechanisms are
increased hydrostatic forces within the
lung microvasculature and increased
microvascular permeability.
29

30. Cardiac Causes
• Pulmonary oedema can occur in heart failure.
• It may be a consequence of conditions like heart
attack severe anemia or diseases of the heart
valves.
• These conditions may cause increased pressure
in the left atrium, which in turn is transmitted to
the lung capillaries.
• The pressure pushes the fluid through the
capillaries into the lung tissue.
30

31. Non-Cardiac Causes
• Infections, damage to lungs caused by smoke or aspiration of stomach contents
into the lungs. These conditions increase capillary permeability.
• Injury to the chest due to trauma.
• Side effects of medications like aspirin or chemotherapy.
• Neurogenic pulmonary oedema, which occurs as a reaction to a condition
affecting the nervous system like trauma, meningitis, etc.
• Re-expansion pulmonary oedema. This type of pulmonary oedema occurs
following treatment of pleural effusion or pneumothorax, which are conditions
where fluid or air accumulates in the pleural space, respectively.
• On treatment of these conditions, a negative pressure is created in the chest,
which could give rise to pulmonary oedema.
31

32. Clinical Manifestations
• Breathlessness on exertion
• Breathlessness on lying down and at night
• Increase in heart rate
• Cough with pink, frothy sputum
• Excessive sweating
• Feeling of anxiety
• Bluish color of the skin due to reduced
oxygen content of blood. (cyanosis)
• Wheezing
32

33. Medical Management
1.Diuretics are used as first line of treatment, and furosemide is the most
commonly used medication. Higher doses are associated with more
improvement in dyspnea, however, also associated with transient worsening of
renal function.
2.Vasodilators can be added as an adjuvant therapy to the diuretics in the
management of pulmonary oedema. IV nitroglycerin is the drug of choice, and
it lowers preload and pulmonary congestion.
• Ventilatory support, both noninvasive and invasive is used to improve
oxygenation, direct alveolar, and interstitial fluids back into the capillaries,
improve hypercarbia and hence reverse respiratory acidosis, and tissue
oxygenation. It also aims at reducing the work of breathing.
33

34. Acute Respiratory Distress Syndrome (ARDS)
• ARDS develops rapidly and includes sever dyspnea, diffuse pulmonary infiltrates
and hypoxemia that typically causes respiratory failure.
• Key Diagnostic Criteria For ARDS Includes :
Diffuse bilateral pulmonary infiltrates on chest x-ray.
Respiratory failure not explained by cardiac failure
Poor oxygenation PaO2/FiO2≤100 mmHG
> 80% of result from pneumonia. Sepsis, multiple blood transfusions, gastric acid
aspiration and drug overdose.
Other Risk Factors: Older Age, Chronic Alcohol Abuse, Metabolic Acidosis,
Severity of a Critical illness.
34

35. • The hallmark of ARDS is
hypoxemia that is
resistant to oxygen
therapy
• Initially compensate by
hyperventilating
• Maintain an acceptable
PaO2 with an acute
respiratory alkalosis.
• Deteriorate over several
hours, requiring
endotracheal intubation
and mechanical
ventilation.
35

36. Etiology
PULMONAR
Y
PNEUMONIA
ASPIRTION
SMOKE INHALATION
O2 TOXICITY
EMBOLI
CONTUSION
RADIATION
DRUGS
EXTRA PULMONARY
BURNS
PANCREATITIS
TRAUMA
SHOCK
NEUROGENIC
CARDIO PULMONARY - BYPASS
ANAPHYLAXIS
36

37. Clinical Course And Pathophysiology
• There are 3 phases in the natural history of ARDS:
1. Exudative Phase: Begins within 12 to 36 hours after inciting insult.
Duration: Typically up to 7 days
Alveolar
Edema +
Inflammation
Atelectasis
Reduced Lung
Compliance
Hypoxemia Tachypnoea
Progressive
Dyspnea
Increased
Pulmonary
Dead Space
37

38. 2. Proliferative Phase: Duration :
From 7th up to 21 days after inciting insult.
Most of the patients recover, whereas few develop progressive lung injury and
eventually it progresses to pulmonary fibrosis.
Dyspnea and hypoxemia persist during this phase.
3. Fibrotic Phase :
Majority of the patients recover in 3 to 4 weeks, the one’s who don’t
experience progressive fibrosis.
Need prolonged ventilator support or supplemental O2.
Increased risk of pneumothorax, reductions in lung compliance and increased
pulmonary dead space.
38

39. 39

40. Medical Management
• Patients with ARDS typically require mechanical ventilatory supports due
to hypoxemia and increased work of breathing.
• In ARDS, alveolar collapse can occur due to alveolar interstitial fluid
accumulation , thus worsening hypoxemia.
• Therefore, low tidal volumes are combined with the use of PEEP at levels
that strive to minimize alveolar collapse and achieve adequate oxygenation.
• Patients with ARDS have increased pulmonary vascular permeability
leading to interstitial and alveolar oedema.
• Therefore they should receive IV fluids only as needed to achieve adequate
cardiac output.
40

41. Physiotherapy Management
• Facilitating mucociliary transport is a primary goal in these patients.
• Impaired mucociliary transport can be precipitated by alveolar hypoventilation.
• Multiple positions, including upright positions and and multiple position changes
facilitates mucociliary transport.
• In the event of mucous accumulation and difficulty in removing pulmonary
secretions, specific body positions are selected to optimize postural drainage of the
affected bronchopulmonary segments and to maximize alveolar volume and
ventilation.
• Suctioning may be most effective immediately before and after position changes.
• Rest as a treatment interventions to enable the patient to physiologically restore
between and within treatments especially for ICU patients who have increased
oxygen demands. 41

42. Respiratory Failure (RF)
• Respiratory failure is defined as inadequate gas exchange due to malfunction
of one or more components of the respiratory system.
• There are 2 main types of respiratory failure : a) Hypoxemia
b) Hypercarbia
Condition in which respiratory system fails in one or both of its gas exchanging
function :
1.Oxygenation
2.CO2 elimination
Acute RF : Life threatening derangements in ABG and acid base status.
Chronic RF : Manifestations are clinically inapparent.
42

43. Classification Of Respiratory Failure
• Type 1 - (hypoxemic) respiratory failure has a PaO2 < 60 mmHg with normal
or subnormal PaCO2. In this type, the gas exchange is impaired at the level of
alveoli-capillary membrane. Examples of type I respiratory failures
are carcinogenic or non-cardiogenic pulmonary oedema, COVID-19 and
severe pneumonia.
• Type 2 - (hypercapnic) respiratory failure has a PaCO2 > 50 mmHg.
Hypoxemia is common, and it is due to respiratory pump failure.
43

44. 44

45. Pathophysiology
• Hypoventilation: in which PaCO2 and PaO2 and alveolar-arterial PO2 gradient
(difference between the calculated oxygen pressure available in the alveolus and
the arterial oxygen tension, measures the efficiency of gas exchange). are normal.
Depression of CNS from drugs (eg opioid use disorder) is an example of this
condition.
• V/P mismatch: this is the most common cause of hypoxemia.
• These two variables, V & Q, constitute the main determinants of the blood oxygen
(O2) and carbon dioxide (CO2) concentration.
• Shunt : In cases of a shunt, the deoxygenated blood (mixed venous blood)
bypasses the alveoli without being oxygenated and mixes with oxygenated blood
that has flowed through the ventilated alveoli, and this leads to hypoxemia in cases
of pulmonary oedema (cardiogenic or noncardiogenic), pneumonia
and atelectasis..
45

46. Clinical Manifestations
• Dyspnoea
• Tachypnoea
• Restlessness
• Confusion
• Anxiety
• Cyanosis- central
• Tachycardia
• Pulmonary hypertension
• Loss of consciousness
46

47. • Signs and symptoms of RF Type I (Hypoxemia) include:
• Dyspnea, irritability
• Confusion
• Tachycardia
• Tachypnoea
• Cyanosis
• Signs and symptoms of RF Type II (Hypercapnia) include:
• Change of behaviour
• headache
• Coma
• Warm extremities
47

48. Medical Management
1.Correction of Hypoxemia
• Adequate tissue oxygenation is to be maintained.
• Inspired oxygen concentration should be adjusted at the lowest level, which is
sufficient for tissue oxygenation.
• Oxygen can be delivered by several routes depending on the clinical situations in
which we may use a nasal cannula, simple face mask , nonrebreathing mask, or high
flow nasal cannula.
2. Correction of hypercapnia and respiratory acidosis
• This may be achieved by treating the underlying cause or providing ventilatory
support.
3. Ventilatory support for the patient with respiratory failure
48

49. Physiotherapy Management
• Physiotherapy treatment will aim to maximize function in pump and
ventilatory systems and improve quality of life.
• In mechanically ventilated patients, early physiotherapy has been
shown to improve quality of life and to prevent ICU-associated
complications like de-conditioning and ventilator dependency.
• Main indications for physiotherapy are excessive pulmonary
secretions and atelectasis.
• Timely physical therapy interventions may improve gas exchange and
reverse pathological progression thereby avoiding ventilation.
49

50. Positioning
• The use of specific body position aim at improving
ventilation/perfusion(V/Q) matching, promoting mucociliary clearance,
improving lung volumes and reducing the work of breathing.
• These include Prone: helps to improve V/Q matching in patients with acute
respiratory distress syndrome. It has been shown to result in oxygenation of
patients with severe acute respiratory failure.
• Side-lying: with affected lungs uppermost to improve aeration through
increased lung volumes in patients with unilateral lung disease.
• Semi-recumbent: 450 head-up position serves to prevent the risk of
gastroesophageal reflux and aspiration.
• Upright: helps to improve lung volumes and decrease work of breathing in
patients that are being weaned from mechanical ventilator.
50

51. • Postural drainage and Percussion: Uses gravitational effects to facilitate
mucociliary clearance.
• Suction: Used for clearing secretions when the patient cannot do so
independently.
• Active cycle of breathing technique and manual techniques such as
percussions and vibration to facilitate mucus clearance.
• Limb exercises: passive, active-assisted, active exercises may optimize
oxygen transport and reduce the effects of immobility.
• Inspiratory muscle training: aims to improve inspiratory muscle strength
and it facilitates weaning from mechanical ventilation. It has be shown to
improve whole body exercise performance.
• Early mobilization: Improves function, mobility and quality of life.
51

52. Pulmonary Embolism
• Pulmonary embolism (PE) is a blockage of one of the pulmonary arteries in the
lungs. In most cases, a thrombus forms in the leg.
• Once dislodged, the thrombus travels to the lungs where it occludes the pulmonary
artery. The condition is a medical emergency that requires prompt diagnosis and
treatment to ensure patient survival.
• Thrombus formation occurs due to stasis in the deep veins, especially at the calf.
The patient's initial cardiorespiratory status, and size and number of emboli affects
the severity of changes in pulmonary blood flow and respiration.
• A small blockage of the pulmonary artery may not provoke symptoms, while a
large embolus can be fatal.
52

53. Risk Factors
• Serious limb injury, surgery, prolonged bed rest, and static lower limb
posture for more than 6 hours
• Trauma and spinal cord injury
• Smoking
• Cancer
• Chemotherapy
• Advanced age (>40 years old)
• Immobilizer or cast
53

54. Clinical Manifestations
• Dyspnea and/or Tachypnoea
• Crackle lung sound on chest
auscultation
• Pleuritic chest pain
• Profuse sweating
• Cough with haemoptysis
• Tachycardia
• Hypotension, dizziness (induced
by exercise only)
• Syncope
• Cyanosis
54

55. Medical Management
• Anticoagulant Therapy
• Fast-acting fibrinolytic agents such as heparin or Penta saccharide are
administered.
• These medications are prescribed with the goal of preventing blood clot
progression.
• Thrombolytic Therapy
• In the case of massive PE, thrombolytic therapy may be indicated.
• Thrombolytic agents work by breaking up obstructive thrombi to restore blood
flow to tissues, and is often used in combination with anticoagulants. The most
widely used medications are streptokinase and urokinase.
55

56. Physiotherapy Management
• Mobility is vital to patient recovery.
• Following anticoagulation and thrombolytic therapies, bed rest is typically
prescribed followed by inpatient therapy.
• Bed mobility exercises are mandatory to prevent deconditioning but aggressive
active range of motion exercises are contraindicated in order to prevent the
dislodgement of the thrombus which could in turn lead to further
complications.
• The main aim of physiotherapy is to restore a clear lung field and oxygen
uptake to optimal level.
• This can be achieved through chest physiotherapy comprising of breathing
exercises as well as percussions and chest vibrations , to make sure that the
patient has a clear chest.
56

57. Stroke / Cerebrovascular Accident
• Abrupt onset neurological disorder of vascular aetiology.
• Nature- Haemorrhagic or Ischaemic in nature.
Types Of Haemorrhagic
Stroke
• Primary Intracerebral
Haemorrhage
• Subarachnoid Haemorrhage
• Primary Intraventricular
Haemorrhage
Types of Ischaemic Stroke
• Lacunar Infarcts
• Transient Ischaemic Attack
• Watershed Infarcts
57

58. 58

59. 59

60. Pathophysiology
Ischaemic Stroke
• Degree of impairment of Cerebral
Blood Flow.
• Thromboembolic arterial
occlusion.
• Neurons are hypoxic, undergo
necrosis.
• Cellular Destruction
Intracerebral
Haemorrhage
• Haematoma growth.
• Maximum growth in the initial 1
hour.
• Haematoma expansion.
• Ischaemia
60

61. Clinical Features Of Stroke
• Muscular: Difficulty in walking ( due to
myalgia).
Problems associated with
coordination.
Hemiplegia/Hemiparesis.
• Visual: Blurred vision, diplopia, temporary
loss of vision.
• Whole body Fatigue.
• Facial: Muscle weakness, Numbness.
• Sensory: Reduced sensation of Touch.
• Speech: Difficulty in speaking, slurred
speech.
• Others: Difficulty in swallowing, headache,
confusion.
61

62. Medical Management
• Positioning- Head of the bed should be flat.
• Calculate ABCD2 Score, if 4 or above-
Administer Asprin 75 to 300mg OD.
• Correct the risk factors : Treatment of
Hypertension, Diabetes, Hyperlipidaemia
and Cessation of Smoking.
• Surgery- If carotid artery TIA : Carotid
Endarterectomy / Stenting.
62

63. Physiotherapy Management
1. Patient Education and Psychological Support
2. Work on normalizing tone and length –Roods Technique and Electrical
stimulation
3. To prepare the postural system for the Upper extremity skills- Train for Trunk
Control
4. Train for Balance and Coordination- Wabble Board Training, Equilibrium and
Non-Equilibrium Exercises and Frenkel’s Exercises.
5. Give opportunities for problem solving, cognitive challenges: Virtual reality,
Mirror therapy.
6. Gait Training- Walker, Parallel Bars.
63

64. Increased Intracranial Pressure and Head Trauma
• ICP is the pressure exerted by the contents inside the cranial vault-the brain tissue
(gray and white matter), CSF, and the blood volume.
• Increased intracranial pressure is defined as cerebrospinal fluid pressure greater
than 15 mm Hg.
64

65. 65

66. Pathophysiology
When this volume-pressure relationship becomes unbalanced , ICP
increases
An increase in the volume of any one component must be accompanied
by a reciprocal decrease in one of the other components
Due to etiological factors
Components of ICP disturbed Brain tissue, CSF, Blood Volume
66

67. Clinical Manifestations
• Headache
• Nausea
• Vomiting
• Increased blood pressure
• Decreased mental abilities
• Confusion
• Double vision
• Shallow breathing
• Loss of consciousness
• Coma
67

68. Medical Management
• Drain CSF via ventriculostomy.
• Elevate head of the bed, midline head
position.
• Corticosteroids- Dexamethasone
• Osmotic diuretic- Mannitol
• Anti-epileptic drugs- Diazepam,
Clonazepam
• Surgical management - decompressive
craniotomy
68

69. Traumatic Brain Injury
Traumatic Brain Injury is a condition in which an insult to the brain is caused due to
any external force , which usually leads to an alteration in the state of consciousness
in the person that in turn impairs the cognitive and physical function along with
behavioural or emotional disturbance.
Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain
from an external mechanical force, possibly leading to permanent or temporary
impairment of cognitive, physical, and psychosocial functions, with an associated
diminished or altered state of consciousness.
Based on Clinical Type : a) Open
b) Closed
69

70. Etiology
• Motor vehicle accidents.
• Falls.
• Sports related injuries.
• Highest among adolescents, young
adults, and those older than 75
years of age.
• Vehicle crashes are the leading
cause of brain injury.
• Falls are the second leading cause.
70

71. Pathophysiology
• Primary Lesions
1. Diffuse Neuronal Damage
2. Shearing Lesions
3. Contusions and Lacerations
• Secondary Lesions
1. Swelling
2. Haemorrhage
71

72. Medical Management
• Resuscitation and Support:
1. Admission Is Indicated When:
Definite history of unconsciousness.
Fractured temporal lobe.
Patient is hypoxic- Endotracheal intubation.
2. Neurological Assessment by Glasgow
Coma Scale
3. Care of unconscious patient:
a) Ryle’s Tube for feeding.
b) Catheter for drainage of urine.
c) Change of position to avoid bed sores.
72

73. Surgical Management
• Indication of surgical decompression:
• The GCS score decreases by 2 or more points between the time of injury and
hospital evaluation.
• The patient presents with fixed and dilated pupils.
• The intracranial pressure (ICP) exceeds 20 mm Hg
• Craniectomy – Excision into the cranium to cut away a bone flap
• Cranioplasty - surgical repair of a defect or deformity of a skull
73

74. Physiotherapy Management
• Respiratory Care
• Preventing Contractures and Deformities
• Prevention and Treatment of Pressure Sores
Management of
Unconscious Patient
• Improve Alertness or Arousal through Sensory Stimulation
• Prevention of Spasticity
• Maximize Patient’s Functional Capacity
• Development of High Level Skilful Functioning
Management of
Conscious Patient
74

75. Other Precautions To Be Taken
• Keep head of bed slightly elevated and the head in midline (straight).
• Avoid range-of-motion exercises until ICP approaches normal.
• Tilt or turn client from side to side every 2 hours.
• Avoid friction by using a lift sheet. - Use a pressure-relieving mattress or air
bed for bed ridden patients.
• Keep skin clean and dry
75

76. Hypoxic Ischaemic Encephalopathy (HIE)
• Hypoxic ischemic encephalopathy (HIE) is one of the most serious
birth complications affecting full term infants.
• It occurs in 1.5 to 2.5 per 1000 live births in developed countries.
• HIE is a brain injury that prevents adequate blood flow to the infant’s
brain occurring as a result of a hypoxic-ischemic event during the
prenatal, intrapartum or postnatal period.
• By the age of 2 years, up to 60% of infants with HIE will die or have
severe disabilities including mental retardation, epilepsy, and cerebral
palsy (CP).
76

77. Causes of Hypoxic Ischaemic Encephalopathy
• Severity of oxygen deprivation: If oxygen deprivation was lengthy or
entirely cut off, there is a greater chance of brain injury.
• How long the baby was deprived oxygen: The longer a baby goes without
adequate oxygen, the more likely he or she will have permanent brain damage.
• The overall condition of the baby: Babies who are premature or who have
other medical conditions are more fragile and vulnerable to brain injury from
a lack of oxygen.
• How the baby’s care is managed: Recognizing and immediately treating
oxygen deprivation is the key to preventing complications and permanent
brain injury damage.
77

78. Antepartum causes: Intrapartum causes: Postpartum causes:
Maternal diabetes with vascular
disease
Excessive bleeding from the placenta. Severe cardiac or pulmonary disease.
Congenital infections of the fetus Maternal low blood pressure Serious Infections, including sepsis and
meningitis.
Problems with blood circulation to the
placenta
Umbilical cord collapse or prolapse. Severe prematurity
Preeclampsia Prolonged late stages of labor. Low neonatal birth weight.
Drug and alcohol abuse Abnormal fetal presentation Brain or skull trauma.
Severe fetal anemia Ruptured placenta or uterus. Respiratory failure.
78

79. Clinical Manifestations
• Low Apgar scores, <5 at 5 minutes and 10 minutes.
• Floppiness, or unreactive to sights or sounds, or more tense and agitated.
• Low heart rate.
• Low blood pressure.
• Poor muscle tone.
• Weak breathing, no breathing at all, or rapid breathing.
• Need for resuscitation after delivery.
• Weak cry.
• Bluish or pale skin color.
• Excessive acid in the blood.
79

80. 80

81. Medical Management
• Mechanical ventilation to help a baby who
can’t breathe without assistance.
• Cooling, or therapeutic neonatal
hypothermia. Therapeutic hypothermia
lowers the baby’s body temperature in order
to reduce swelling and brain injuries. Also
called whole body hypothermia, the
American Academy of Pediatrics considers
this one of the best treatment options to
protect the baby’s brain.
• Medications to control seizures, the baby’s
heart rate and blood pressure.
81

82. 82

83. Physiotherapy Management
• Mobility is vital to patient recovery.
• Bed mobility exercises are mandatory to prevent deconditioning but
aggressive active range of motion exercises are preferred if the child is
active. If not the therapist should make sure that all the range of motion
exercises are performed passively.
• The aim of physiotherapy is to restore a clear lung field and oxygen uptake to
optimal level, which has been lost due to hypoxia.
• This can be achieved through chest physiotherapy comprising of breathing
exercises as well as percussions and chest vibrations , to make sure that the
patient has a clear chest.
• The child can be given medications through the means of nebulization in
order to assist mucocilliary clearance in case the child has secretions.
83

84. EVIDENCES
Title Aim Methodology Conclusion
Standardized Rehabilitation
and Hospital Length of Stay
Among Patients With Acute
Respiratory Failure: A
Randomized Clinical Trial
(2019)
To compare standardized
rehabilitation therapy (SRT) to
usual ICU care in acute
respiratory failure.
Adult patients (mean age, 58
years; women, 55%) admitted
to the ICU with acute
respiratory failure requiring
mechanical ventilation were
randomized to SRT (n=150) or
usual care (n=150) with 6-
month follow-up. Patients in
the SRT group received daily
therapy until hospital
discharge, consisting of
passive range of motion,
physical therapy, and
progressive resistance
exercise. The usual care group
received weekday physical
therapy.
Among patients hospitalized
with acute respiratory failure,
SRT compared with usual care
did decreased hospital length
of stay.
84

85. Title Aim Methodology Conclusion
A Twelve-Week Moderate
Exercise Programme
Improved Symptoms of
Depression, Insomnia, and
Verbal Learning in Post-
Aneurysmal Subarachnoid
Haemorrhage Patients: A
Comparison with
Meningioma Patients and
Healthy Controls. (2020)
The aim of the study was to
compare the effects of an
exercise programme in one
healthy population (control
group) with another patient
group (treatment group).
The study explored the
effects of 12 weeks of
moderate aerobic exercise
training on 15 SAH patients,
16 meningioma patients, and
17 healthy controls. Data on
symptoms of depression,
hypochondria, perceived
stress, satisfaction with life,
verbal learning, memory, and
sleep, were gathered at
baseline, following
intervention, and at 6-month
follow-up.
An exercise programme had a
positive effect on symptoms
of depression, insomnia, and
verbal learning in patients
following SAH. No positive
changes in other domains
were observed. This may be
due to the cautious approach
taken with regard to exercise
intensity.
85

86. Title Aim Methodology Conclusion
Impact of Very Early Physical
Therapy During Septic Shock
on Skeletal Muscle: A
Randomized Controlled
Trial. (2018)
As the catabolic state
induced by septic shock
together with the physical
inactivity of patients lead to
the rapid loss of muscle
mass and impaired function,
the purpose of this study
was to test whether an early
physical therapy during the
onset of septic shock
regulates catabolic signals
and preserves skeletal
muscle mass.
Adult patients admitted for
septic shock within the first
72 hours. Interventions:
Patients were assigned
randomly into two groups.
The control group benefited
from manual mobilization
once a day. The intervention
group had twice daily
sessions of both manual
mobilization and 30-minute
passive/active cycling
therapy.
Early physical therapy
during the first week of
septic shock is safe and
preserves muscle fiber
cross-sectional area.
86

87. Title Aim Methodology Conclusion
Rehabilitation Practices in
Patients With Moderate and
Severe Traumatic Brain
Injury. (2019)
To characterize the
indications, timing, barriers,
and perceived value of
rehabilitation currently
provided for individuals with
moderate or severe
traumatic brain injury (TBI)
admitted to the intensive
care unit (ICU) based on the
perspectives of providers
who work in the ICU.
A survey of the timing of
rehabilitation for patients
with TBI in the ICU was done.
Sixty-six respondents who
reported caring for patients
with TBI in the ICU
completed the survey; 98%
recommended rehabilitative
care while patients were in
the ICU. Common reasons to
wait for the initiation of
physical therapy were
normalization of intracranial
pressure and hemodynamic
stability.
The majority of providers
caring for patients with TBI in
the ICU support
rehabilitation efforts,
typically after a patient is
extubated, intracranial
pressure has normalized, and
the patient is
hemodynamically stable.
87

88. Title Aim Methodology Conclusion
Effects of Early Exercise
Rehabilitation on Functional
Recovery in Patients with
Severe Sepsis. (2018)
To assess the effects of early
exercise rehabilitation on
functional outcomes in
patients with severe sepsis.
A prospective, case-control
study was conducted between
January 2013 and May 2014 at
a tertiary care center in Korea.
Patients with severe sepsis
and septic shock were
Intervention involved early
targeted physical
rehabilitation with sepsis
treatment during
hospitalization. Participants
were assessed at enrollment,
hospital discharge, and 6
months after enrollment.
Functional recovery was
measured using the Modified
Barthel Index (MBI),
Functional Independence
Measure (FIM), and
Instrumental Activities of Daily
Living (IADL).
Early physical rehabilitation
may improve functional
recovery at hospital discharge,
especially in patients with
high initial severity scores.
88

89. Title Aim Methodology Conclusion
Effect of early
rehabilitation exercise
on blood pressure of
elderly patients with
septic shock: a single-
center, prospective,
randomized controlled
study. (2021)
To observe the effect of
early rehabilitation
exercise on blood
pressure of elderly
patients with septic
shock.
A single-center, prospective, randomized
controlled study was conducted in elderly
patients with septic shock who were hospitalized
in the department of critical care medicine of
Huangshan Shoukang Hospital . All patients were
divided into control group and intervention
group. Both groups were treated with lower limb
barometry to prevent deep vein thrombosis, 3
times a day, 30 minutes each time. After
comprehensive treatment in the intensive care
unit (ICU), the severity of patients was gradually
improved, the hemodynamics was relatively
stable, and the norepinephrine was reduced. The
control group continued to receive lower limb
barometric treatment without rehabilitation
training, while the intervention group began
rehabilitation The duration of norepinephrine
use, the length of ICU stay, and the occurrence of
adverse events during rehabilitation training in
intervention group was recorded.
The early rehabilitation
exercise was beneficial
to the recovery of
autonomic blood
pressure in elderly
patients with septic
shock, shorten the time
of norepinephrine use
and ICU stay.
89

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• KD Tripathi , Essentials of Medical Pharmacology, 8th Edition.
• K Rajgopal Shenoy, Manipal Manual of Surgery, 4th Edition
• Glady Samuel Raj , Physiotherapy in Neuro Conditions
• Brian R Walker, Davidson’s Principles and Practice of Medicine, International
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• K George Matthew, Medicine Prep Manual for Undergraduates, 4th Edition.
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93. THANK YOU
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