intracranial space-occupying lesions: GROUP 3 SURGERY.pptx

intracranial space-occupying lesions

1. GROUP 3

2. GROUP 3 MEMBERS MINA AMIDU 2405001 PRECIOUS NYIRENDA 2405038 FRANK CHUNGA 2405013 JOSEPH CHIDULE 2405009 HASSINAH MKOLOKOSA 2405032 TSANZO KADZAMIRA 2405021 MAGGRET NKHONJERA 2405037

3. INTRACRANIAL SPACE-OCCUPYING LESIONS(ICSOL)

4. OBJECTIVES By the end of the presentatations everyone should be able to: Define intracranial space-occupying lesions (ICSOL) and describe their consequences. Identify the clinical features of raised intracranial pressure (ICP). Outline the common causes of raised ICP. Explain the assessment of head injury. Classify head injuries using the Glasgow Coma Scale (GCS). Discuss the sequelae of head injury Post-head injury to endocrine complications Post-head injury to autonomic complications. Identify other avoidable causes of death associated with head injury. Summarize the management of head injury Interventions of care in patients with head injuries

5. DEFINITION OF ICSOL Intracranial space-occupying lesions refer to abnormalities within the cranial cavity that take up space and can exert pressure on surrounding brain tissue. These lesions can have various consequences depending on their nature, location, size, and growth rate. TYPES OF LESIONS 1. Tumors: Primary brain tumors (e.g., gliomas, meningiomas ) or metastatic tumors from other cancers. 2. Abscesses: Collections of pus due to infection. 3. Hematomas: Blood collections due to trauma or vascular issues. 4. Cysts: Fluid-filled structures.

6. CONSEQUENCES 1. Increased Intracranial Pressure (ICP): Space-occupying lesions can elevate ICP, leading to symptoms like headache, nausea, vomiting, and papilledema. 2. Neurological Deficits: Depending on location, lesions can cause motor weakness, sensory changes, speech disturbances, visual disturbances, or seizures. 3. Brain herniation: Severe increases in ICP can lead to brain herniation, a life-threatening emergency where brain tissue is displaced across structures like the tentorium or foramen magnum.

7. Conti; 4. Cognitive and Behavioral Changes: Lesions affecting specific brain areas can lead to changes in cognition, personality, or behavior. 5. Hydrocephalus: Obstruction of CSF pathways can lead to hydrocephalus (accumulation of cerebrospinal fluid). 6. Decreased cerebral perfusion: high ICP can reduce blood flow to the brain, leading to ischemia or further damage

8. CLINICAL FEATURES OF RAISED ICP Headache: Often worse in the morning. Vomiting: it is projectile due to increased ICP Seizures: Depending on lesion location and type. Focal Neurological Signs: Vary based on lesion location (e.g., hemiparesis, aphasia). Papilledema due to optic disc swelling Altered consciousness ( confusion, drowsiness, coma) Cushing's triad: bradycardia, hypertension and irregular breathing

9. THE COMMON CAUSES OF ICP Traumatic Brain Injury (TBI) A blow to the head can cause bleeding and swelling within the skull, leading to increased pressure. Hematomas These are collections of blood that can form in or around the brain, such as subdural hematomas or epidural hematomas. Stroke A stroke, particularly when it involves bleeding in the brain (hemorrhagic stroke), can pool blood and increase pressure. Aneurysm Rupture The rupture of an aneurysm can lead to bleeding into the brain and surrounding areas. .

10. CONTI; Brain Tumors Tumors can take up space and restrict blood flow, leading to increased pressure. Abscesses Pockets of infection or pus within the brain can also act as space-occupying lesions Infections: 1. Meningitis An infection of the membranes covering the brain and spinal cord can cause swelling and irritation. 2. Encephalitis: Inflammation or swelling of the brain itself is another cause of increased ICP.

11. CONTI ; Fluid and Swelling Issues: Hydrocephalus: An increase in cerebrospinal fluid (CSF) within the brain's ventricles can build up pressure. Cerebral Edema: Swelling of the brain tissue itself can increase the volume within the skull. Other Conditions: Seizures : Seizures can sometimes lead to increased ICP. High Blood Pressure (Hypertension): This can lead to bleeding in the brain, contributing to increased pressure. Toxin Buildup: Conditions like kidney failure can lead to an accumulation of toxins (uremic encephalopathy) or ammonia (hyperammonemia), which can affect brain function and increase

12. ASSESSMENT OF HEAD INJURY Primary survey (ABCDE approach) Glasgow Coma Scale (GCS) Neurological examination Imaging (CT, MRI) History( mechanism, loss of consciousness, vomiting, seizures)

13. PRIMARY SURVEY ( ABCDE) AIRWAY Ensure the airway is clear and patent. Look for obstruction: blood, vomit, tongue, swelling. If the patient is talking → airway is patent. Protect cervical spine in trauma (apply collar, manual in-line stabilization). Interventions: suction, airway adjuncts (oropharyngeal, nasopharyngeal, endotracheal tube).

14. 2. BREATHING Assess breathing and oxygenation. Look: chest movements, injuries (flail chest, penetrating trauma). Listen: breath sounds (equal or reduced). Feel: air entry, chest expansion. Monitor respiratory rate, oxygen saturation. Interventions: give high-flow oxygen, support ventilation if inadequate (bag-mask ventilation, mechanical ventilation).

15. 3. CIRCULATION Assess circulation and perfusion. Check pulse (rate, rhythm, strength), blood pressure, capillary refill. Look for signs of external or internal bleeding. Insert IV access, take blood samples. Interventions: control bleeding, give IV fluids or blood transfusion if needed.

16. 4. DISABILITY (NEUROLOGICAL STATUS ) Quick neurological evaluation: Level of consciousness (Glasgow Coma Scale). Pupillary size and reaction. Blood glucose (to rule out hypoglycemia). Interventions: treat reversible causes (low sugar, seizures, hypoxia).

17. 5.EXPOSURE / ENVIRONMENT Fully expose the patient to look for hidden injuries (while preventing hypothermia). Check for other injuries, rashes, bleeding, bruising. Maintain patient’s dignity and warmth with blankets.

18. GLASGOW COMA SCALE (GCS) It assesses the severity of a head injury by rating eye opening, verbal responses, and motor response with a total score from 3 to 15. WHY IS IT IMPORTANT IN ASSESING THE HEAD INJURIES? I nitial Severity Assessment: It provides an initial, standardized assessment of the patient's level of consciousness. Guidance for Treatment: A low score (≤8) indicates a severe brain injury and signifies the need for immediate medical attention, including airway management. Prognosis and Monitoring: The GCS score is used to predict short-term and long-term outcomes and to monitor a patient's neurological status, with changes in the score over time being more significant than the absolute value.

19. Interpreting the Scores the total GCS score is the sum of the points from each of the three responses. Total score 13–15: Mild head injury Total score 9–12: Moderate head injury Total score 3–8: Severe head injury

20. Neurological examination Key Components of a Neurological Exam 1. Glasgow Coma Scale (GCS): A standardized 15-point scale that assesses eye-opening, verbal response, and motor response, with scores from 3 to 15 indicating severity, with higher scores meaning less severe injury. 2. Mental Status: Evaluates level of consciousness, orientation (person, place, time), attention, memory, and cognitive function. 3. Cranial Nerves: Assesses pupil size and response to light, eye movements, facial strength, and other functions controlled by the cranial nerves. This is crucial for detecting brainstem dysfunction. 4. Motor Examination: Checks for muscle tone and strength, coordination (e.g., finger-to-nose test), and the ability to move limbs.

21. Conti; 5. Sensory Examination: Evaluates the ability to perceive sensations such as heat or a needle prick, typically in a non-conscious patient. 6. Reflexes: Deep tendon reflexes are tested to assess spinal nerve motor and sensory function. WHY IS NEUROLOGICAL EXAMINATION IMPORTANT? Determines Severity: The GCS and other parts of the exam help doctors quickly assess the severity of the brain injury. Identifies Brainstem Damage: Cranial nerve examination provides crucial information about potential damage to the brainstem.

22. IMAGING ( CT, MRL 1. COMPUTED TOMOGRAPHY (CT) Role: The imaging test of choice in the acute phase of head trauma to rapidly identify life-threatening conditions. What it shows: Skull fractures Bleeding in the brain (intracranial hemorrhages) Blood clots (hematomas) Brain tissue swelling (edema) and bruising (contusions) Mass effect (pressure on brain structures) It quick, readily available, and excellent at visualizing bone and detecting acute bleeding.

23. KEY INDICATORS FOR A CT SCAN

24. Conti; 2. MAGNETIC RESONANCE IMAGING (MRI) Role: Typically performed after the initial stabilization or in cases where symptoms persist or don't improve after a CT. It is also preferred for subacute and chronic stages of injury. What it shows: More detailed views of brain tissue and can be better for identifying certain internal brain injuries or delayed onset of damage. It provides superior detail for soft tissues, which can be crucial for assessing injuries not clearly seen on CT.

25. HISTORY Key Areas to Assess Mechanism of Injury How did the injury occur? Was it a fall, a high-energy trauma like a road traffic accident, or something else? Loss of Consciousness Was there any period of altered consciousness, and if so, how long did it last? Amnesia Was there any loss of memory for events before or after the injury? Sequence of Events What happened immediately before, during, and after the injury?

26. Conti; Symptoms The symptoms like dizziness, nausea, or confusion Headache Is there a persistent headache, which could indicate a more serious issue? Vomiting Any episodes of vomiting since the injury? Pre-Existing Medical History Any known neurological conditions, such as epilepsy? Any bleeding or clotting disorders? Previous head injuries or brain surgery? Medications and Substances: Current medications, especially anticoagulants or antiplatelet drugs?

27. CLASSIFICATION OF HEAD INJURIES USING THE GLASGOW COMA SCALE (GCS). 1. Mild Head Injury GCS: 13–15 Features: Patient may be awake and responsive, may have transient confusion, dizziness, headache, or brief loss of consciousness (<30 minutes). 2. Moderate Head Injury GCS: 9–12 Features: Patient may be drowsy, confused, or have longer periods of unconsciousness. Risk of complications like brain swelling or bleeding is higher.

28. Conti ; 3. Severe Head Injury GCS: 3–8 Features: Patient is in coma or unconscious, does not follow commands, may require airway support and urgent neurosurgical intervention.

29. THE SEQUELAE (CONSIQUENCES)OF HEAD INJURY These are issues or problems that rise from brain damage and can lead to long-term health problems and challenges in daily functioning. Physical sequelae Cognitive sequelae Psychiatric and behavioral sequelae Sleep disorders Long- term concerns

30. 1. PHYSICAL SEQUELAE Headaches and Dizziness: Persistent headaches and feelings of dizziness are common after head injuries. Vision Problems: Difficulty with eye movements, blurry vision, and increased eye strain can occur. Cranial Nerve Damage Injuries to the skull base can affect cranial nerves, leading to symptoms like double vision, loss of smell, or facial paralysis. Spasticity: Increased muscle tone and spasms can develop, impacting mobility and daily activities. Infections Fractures can create openings for bacteria, leading to serious infections like meningitis or brain abscesses.

31. 2. COGNITIVE SEQUELAE Memory and Attention Deficits: Difficulty with memory, concentration, and maintaining attention are frequent after a TBI. Executive Function Impairment: Problems with planning, organization, and other "frontal" functions can emerge. Slowed Information Processing: The speed at which information is processed can be significantly reduced.

32. 3. PSYCHIATRIC AND BEHAVIORAL SEQUELAE Mood Disorders: Depression, anxiety, and mood swings are common. Apathy and Disinhibition: Patients may experience a lack of interest or show inappropriate, uninhibited behavior. Aggression and Impulsivity: Increased impulsivity and aggressive tendencies can arise from damage to frontal and temporal areas of the brain. Psychotic Syndromes: In some cases, head injuries can be associated with psychosis.

33. 4. Sleep disorders Insomnia Difficulty falling asleep or staying asleep. Can be caused by pain, anxiety, or changes in routine following the injury. Hypersomnia Excessive daytime sleepiness, leading to prolonged naps or difficulty staying awake. May result from fatigue or disruptions in sleep architecture Sleep Apnea Obstructive sleep apnea may occur due to changes in brain function or weight gain after injury. Symptoms include loud snoring, gasping during sleep, and daytime fatigue. Circadian Rhythm Disorders Disruption of the body’s natural sleep-wake cycle, leading to irregular sleep patterns. Often seen in those with cognitive impairments or mood disorders.

34. 5. LONG-TERM CONCERNS Increased Risk of Neurodegenerative Disease Research suggests that TBI ( traumatic brain injury ) may inhibit a crucial cell-cleaning process called autophagy, potentially linking it to the later development of neurodegenerative diseases like Alzheimer's and Parkinson's. Functional Impairment The combined cognitive and behavioral deficits can make it difficult to work, manage finances, or handle other aspects of daily life.

35. POST HEAD INJURY- ENDOCRINE COMPLICATIONS Pathophysiology of Endocrine Dysfunction Post-Head Injury The hypothalamic-pituitary (H-P) axis is highly susceptible to injury because of its anatomical location and vascular supply. The pathophysiological mechanisms include: Mechanical Damage : Direct trauma can cause shearing or compression of the hypothalamus or pituitary stalk. Vascular Injury : Damage to blood vessels supplying the hypothalamic-pituitary region can lead to ischemia and necrosis. Secondary Effects : Oedema, increased intracranial pressure, and secondary inflammatory responses may further impair hormone secretion.

36. Cont’………. Disruption of Neurosecretory Pathways : Injury to hypothalamic nuclei or axons disrupts releasing and inhibiting hormones' transport to the anterior pituitary. Extent of Damage : The severity and location of injury determine the specific hormonal deficits. For example, damage to the pituitary stalk often results in multiple hormone deficiencies. The clinical significance depends on the extent of damage and individual patient factors, but early injury often results in transient or permanent neuroendocrine deficiencies.

37. COMMON ENDOCRINE DISORDERS POST-TRAUMATIC HEAD INJURY 1. Hypopituitarism Defined as decreased secretion of one or more hormones from the anterior pituitary. Commonly includes deficiencies in growth hormone (GH), adrenocorticotropic hormone (ACTH), gonadotropins (LH & FSH), and thyroid-stimulating hormone (TSH). Symptoms are often subtle or nonspecific, including fatigue, weakness, depression, and sexual dysfunction. Prevalence varies widely, with some studies reporting up to 30-50% in severe TBI cases.

38. Cont ’….. 2. Diabetes Insipidus (DI) Caused by deficiency of antidiuretic hormone (ADH) or vasopressin. Presents with polyuria (large urine output), polydipsia, hypernatremia, and dehydration. Usually occurs acutely following trauma due to injury to the posterior pituitary or hypothalamus. Management includes desmopressin and careful fluid balance. 3. Gonadotropin Deficiency Leads to hypogonadism, affecting libido, sexual function, and fertility. Can cause amenorrhea in women and decreased libido in men.

39. Cont ’…. 4. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Excessive ADH secretion leads to water retention, hyponatremia, and concentrated urine. May complicate the clinical course, especially in the subacute phase. Symptoms include headache, nausea, confusion, and in severe cases, seizures. Management involves fluid restriction and addressing the underlying cause.

40. Cont ’…… 5. Adrenal Insufficiency Due to impaired adrenocortical-tropic hormone (ACTH) secretion, leading to cortisol deficiency. Symptoms: fatigue, hypotension, hypoglycaemia, abdominal pain. Can be life-threatening if unrecognized; thus, prompt diagnosis is crucial.  6. Thyroid Dysfunction Usually hypothyroidism due to impaired TSH secretion. Transient or persistent. Symptoms: fatigue, cold intolerance, weight gain, depression.

41. POST HEAD INJURY- AUTONOMIC COMPLICATIONS 1. Autonomic Dysregulation (Paroxysmal Sympathetic Hyperactivity - PSH) Seen in severe traumatic head injury. Features includes: Sudden episodes of hypertension, Tachycardia, Hyperthermia, Diaphoresis (excess sweating), Pupil dilation and Dystonia or posturing 2. Neurogenic Shock Results from disruption of sympathetic pathways in high cervical spinal cord or brainstem injuries. Characterized by: Hypotension, Bradycardia and Hypothermia Unlike haemorrhagic shock, skin may be warm and flushed.

42. Cont’…. 3. Cardiovascular Instability Arrhythmias (due to autonomic imbalance). Labile blood pressure (alternating hypo- and hypertension). Risk of sudden cardiac death from excessive sympathetic drive. 4. Thermoregulatory Disturbances Injury to hypothalamus causes: Hyperthermia (due to increased sympathetic activity or hypothalamic damage). Hypothermia (loss of heat regulation). Poikilothermia (body temperature fluctuates with environment).

43. Cont ’… 5. Respiratory Autonomic Dysfunction Abnormal breathing patterns. Loss of protective airway reflexes. Autonomic dysfunction increases risk of aspiration and pneumonia. 6. Gastrointestinal and Urinary Dysfunction Autonomic imbalance may causes: Gastric stasis and paralytic ileus, Neurogenic bladder (urinary retention or incontinence) and Constipation due to impaired parasympathetic tone.

44. OTHER AVOIDABLE CAURSES OF DEATH ASSOCIATED WITH HEAD INJURY 1. Airway obstruction In unconscious patients, the tongue, blood, vomitus, or secretions may block the airway. This is avoidable with early airway management such as suctioning, positioning, or endotracheal intubation. 2. Hypoxia Often results from inadequate airway protection, aspiration, or chest injuries. Providing supplemental oxygen and assisted ventilation can prevent hypoxia-related brain injury and death.

45. Cont ’… 3. Hypotension (shock) Usually due to extracranial bleeding (chest, abdomen, pelvis, or long bones), since isolated head injury rarely causes severe blood loss. Early recognition, fluid resuscitation, and control of bleeding are lifesaving. 4. Raised intracranial pressure (ICP) Develops from cerebral edema, mass effect, or obstructed cerebrospinal fluid pathways. Preventable causes of death if ICP is controlled with head elevation, osmotic therapy (mannitol, hypertonic saline) and timely neurosurgical interventions.

46. Cont ’… 5. Intracranial hematomas Epidural, subdural, and intracerebral hematomas are major avoidable causes of death. For example, an epidural hematoma may present with a "lucid interval" before rapid deterioration. With rapid CT scan diagnosis and urgent surgical evacuation, death can often be prevented. 6. Seizures Post-traumatic seizures increase oxygen demand and can worsen secondary brain injury. Prophylactic anticonvulsants and prompt seizure control help prevent complications.

47. Cont ’… 7. Infection Seen in open skull fractures, penetrating injuries, or CSF leaks, which may lead to meningitis or brain abscess. Preventable with aseptic wound care, antibiotics, and surgical repair where necessary.

48. course prevention Hypoxia & Hypotension Airway management, fluid resuscitation Elevated ICP ICP monitoring, surgical intervention, medications Infections Aseptic techniques, early antibiotics Respiratory complications Skilled airway management, ventilatory support

49. SUMMARY-MANAGEMENT OF HEAD INJURY Primary Survey (ABCDE Approach) Airway: Clear and secure airway, protect cervical spine (immobilization, cervical collar). Breathing: Administer high-flow oxygen, monitor chest movements, SpO₂. Circulation: Control external bleeding, insert large-bore IV lines, give IV fluids or blood Disability: Rapid neurological assessment (Glasgow Coma Scale, pupil size or reactivity) and look for signs of raised intracranial pressure. Exposure: Fully expose the patient to check for other injuries.

50. 2. SECONDARY SURVEY Head-to-toe Evaluation Detailed history (mechanism of injury, loss of consciousness, vomiting, seizures). Full neurological examination (motor, sensory, cranial nerves). Order investigations: CT scan of the head (definitive for hematomas, contusions, skull fractures).Imaging of cervical spine, chest, abdomen if indicated. Monitor vitals and GCS repeatedly.

51. 3. DEFINITIVE MANAGEMENT IN SEVERE CASES Airway and ventilation: Secure airway with intubation, maintain adequate oxygenation and ventilation ICP control: Head elevation 30°. Osmotic therapy (mannitol or hypertonic saline). Avoid hypoxia and hypotension. Seizure prophylaxis: Short-term antiepileptics (e.g., phenytoin or levetiracetam). Neurosurgical intervention: Evacuation of epidural hematoma. Evacuation of subdural hematoma. Decompression for intracerebral hematoma with mass effect. Repair of depressed skull fractures if compressing brain tissue. Suctioning if there is airway obstruction.

52. INTERVATION OF CARE Immediate First Aid Stay still and safe: Do not move the person unless absolutely necessary and always assume the neck is injured. Stop bleeding: Apply firm pressure with a clean cloth, but avoid direct pressure if a skull fracture is suspected. Monitor breathing: Watch for changes in breathing or consciousness and be prepared to start CPR if there are no signs of circulation. Position the head: If the person is vomiting, roll their head, neck, and body together as a unit onto their side to prevent choking. Apply ice: Cover an ice pack in a towel and apply it to swollen areas .

53. Intervention of care conti ’ Medical Interventions Stabilization: Ensuring adequate oxygen and blood supply to the brain. Imaging: Using tools like CT scans to assess the extent of damage and the need for further treatment. Medications: Anti-seizure drugs may be given to prevent secondary damage, and sometimes coma-inducing drugs are used to reduce oxygen demand in the brain. Surgery: May be necessary for severe injuries to repair damage, manage bleeding, or relieve pressure inside the skull. It can also involve tracheotomy and gastrostomy on Observation:

54. Cont’… Long-Term Care & Rehabilitation Physical Therapy Speech Therapy Cognitive Therapy Psychological Counseling Rest What to Avoid; do not remove objects sticking out of a head wound, do not remove a helmet if a serious injury is suspected an do not give sedatives or over-the-counter NSAIDs (like ibuprofen) unless instructed by a doctor, as they can increase bleeding risk.

55. PREVENTABLE FACTORS OF HEAD INJURIES Always wear a seatbelts in vehicles Use age-appropriate car seats or booster seats for children. Prevent falls at home by installing handrails, grab bars, and safety gates. Wear properly fitting helmets when riding bicycles, motorcycles, or playing contact sports. Avoid driving under the influence of alcohol, drugs, or when fatigued. Follow sports safety rules to minimize head impacts.

56. Conclusion In summery understanding intracranial space-occupying lesions and their consequences is critical for timely diagnosis and intervention. Recognizing clinical features of raised intracranial pressure aids in head injury management. The Glasgow Coma Scale is essential for classifying injury severity and guiding treatment. Awareness of head injury sequelae emphasizes the need for comprehensive post-injury care. Addressing preventable causes of death related to head trauma is vital for implementing preventive strategies. Effective management and interventions are key to optimizing outcomes, reducing morbidity, and providing holistic care for head injury patients.

57. References Adam, D., & Smith, J. (2019). Neurosurgical emergencies : A comprehensive guide. Oxford University Press. Bogousslavsky, J. (2020). Neurocritical care : From pathophysiology to clinical practice. Springer. Greenberg, M. S. (2021). Handbook of neurosurgery (8th ed.) . Thieme Medical Publishers. Khandelwal, P., & Ramaswamy, K. (2022). Trauma and head injury : An integrated approach. Elsevier. Williams, P. T., & Hopper, A. (2023). Critical care neurology . Academic Press. Yeo, T. T., & Tan, C. H. (2024). Trauma management in neurology and neurosurgery . CRC Press. Zhang, L., & Li, H. (2025). Modern approaches to neurotrauma . Springer.