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Breathing for the Head John Peterson, DO KU School of Medicine - Wichita.

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Presentation on theme: "Breathing for the Head John Peterson, DO KU School of Medicine - Wichita."— Presentation transcript:

1 Breathing for the Head John Peterson, DO KU School of Medicine - Wichita

2 Disclosures I’ve known Alan and Jeff for a while……

3 Objectives Neurological injuries Physiological effects Airway management Ventilator management

4

5 Neurological injuries Disturbances in consciousness Encephalopathy Traumatic brain injury Acute Myelopathy Ischemic stroke Intracerebral hemorrhage Subarachnoid hemorrhage Brain tumors Status epilepticus Venous thrombosis – Cerebral Sinus – DVT/PE Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, pp xi - xiii

6 Disturbances in Consciousness Drowsy Stupor Minimally conscious state Vegetative state – Restored sleep/wake cycle Locked – in syndrome Coma Brain death

7 Encephalopathy Vascular Trauma Neoplasm Seizure Organ Failure Metabolic Endocrine Pharmacologic CNS infection Systemic infection Inflammatory and immune – mediated encephalitis Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 289

8 Traumatic Brain Injury Primary injury Secondary injury – May be more injurious – Hypoxia and hypoperfusion most likely are the most critical factors in secondary injury Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 308

9 Acute Myelopathy Traumatic Degenerative spine Neoplastic Inflammatory Systemic disease Bacterial and viral infections Vascular Toxic/Metabolic

10 Stroke Defined – Focal neurological deficit that has an arterial distribution that correlates with specific region of the brain

11 Normal Brain

12 Ischemic stroke Focal neurological deficit corresponding to arterial territory Transient ischemic attack (TIA) – Symptoms resolve in less than 24 hrs Typically less than 1 hr Reversible Ischemic Neurologic Deficit (RIND) – Symptoms lasting 24 – 72 hrs Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 341

13 Ischemic Stroke

14 Ischemic stroke Embolic – Cardiac – Artery to artery embolus – Paradoxical embolus Thrombotic – Intracranial atherosclerosis – Lipohyalinosis – Arterial dissection – Arteritis – Fibromuscular dysplasia – Vasospasm – Hypercoaguable states Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 342

15 Ischemic Stroke Modifiable – Diabetes mellitus – Hypertension – Smoking – Hypercholesterolemia – Coronary artery disease Non-modifiable – Age – Male – Family history Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 342

16 Intracerebral Hemorrhage

17 10 – 15% of all strokes 30 day mortality: 35 – 52% Only 20% are independent functional at 6 months Etiology – Primary Secondary to hypertension – Secondary Aneurysmal, AVM, Tumor, Amyloid angiopathy, Coagulopathies, Trauma

18 Intraventricular Hemorrhage

19 Subarachnoid Hemorrhage Trauma – Most common cause Spontaneous – 80% Aneurysmal – 10 – 15% Perimesencephalic nonaneurysmal hemorrhage – 5% Nonaneurysmal 2 – 5% of all strokes

20 Subarachnoid Hemorrhage

21 Vasospasm Occurs between days – Lasts up to 21 days Monitoring with transcranial doppler (TCD) Treatment for symptomatic vasospasm – Triple H Hypertension Hypervolemia Hemodilution – Angiography with balloon dilation or intra-arterial calcium – channel blocker infusion

22 Epidural Hematoma Subdural Hematoma

23 Post-Cardiac Arrest Brain Injury Therapeutic hypothermia – Indicated for out-of-hospital ventricular fibrillation arrest – Possible benefit with asystole and PEA – 55% of the hypothermia group had a favorable outcome vs 39% in the normothermia group At 6 months 41% of the hypothermia group died vs 55% of the normothermia group Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 393

24 Venous Thrombosis Cerebral Sinus – Rare cause of stroke Thrombophilia is most common cause Systemic anticoagulation required DVT/PE – 79% of pulmonary embolism originates from a lower extremity deep vein thrombosis – Neurological conditions predisposing to VTE Spinal cord injury Traumatic brain injury Ischemic stroke Intracerebral hemorrhage Malignant glioma Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p ,

25 Venous Thrombosis Deep Vein Thrombosis – Risk Factors Venous valvular insufficiency Right-sided heart failure Postoperative period Prolonged bedrest Extremity trauma Malignancy and cancer therapy Pregnancy and postpartum period Hormone therapy Spinal cord injury History of venous thromboembolism Hypercoagulable state Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p

26 Malignant Hyperthermia Autosomal dominant condition Triggers – Halogenated inhalational anesthetics – Succinylcholine – Extreme stress, vigorous exercise and heat exposure Risk Factors – Myopathies Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 437

27 Malignant Hyperthermia Signs and symptoms – Unexpected rise in end-tidal CO 2 > 55 or PaCO 2 >60 – Increased minute ventilation – Unexplained tachycardia, ventricular tachycardia or fibrillation, labile blood pressure, congestive heart failure – Metabolic acidosis with elevated serum lactate – Altered mental status (when anesthetic is stopped) – Generalized muscle rigidity, masseter rigidity (despite neuromuscular blockade), rhabdomyolysis – Acute renal failure – Hyperkalemia – Hyperthermia (Temperature can rise 1 – 2 C˚ q 5 min up to 44˚C) This is a late finding – DIC Especially with temp > 41˚C Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 438

28 Malignant Hyperthermia Management – Stop offending agent – Admit to ICU – Increase minute ventilation to normalize PaCO 2 – Body cooling NG icy lavage, ice packs, fans, surface or invasive cooling systems Target temp of 38.5 – Dantrolene Continue for 3 days IV or PO dosing Monitor for excessive muscle weakness or hepatotoxicity – Monitor for recrudescence Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 438

29 Neuroleptic Malignant Syndrome Risks – Prior physical exhaustion and dehydration – Previous episode of NMS – Exposure to antipsychotic drugs Signs and symptoms – Develop within 24hrs – 1 month after exposure to antipsychotic drugs – Regression within 1 wk – 1 month after discontinuation of drug 10% Mortality Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p

30 Brain Tumors Second most common cause of death from intracranial disease 33% overall 5 year survival 33% of all tumors are gliomas – 67% are high grade Metastatic tumors are the most common brain neoplasm – Lung (18 – 64%) – Breast (2 – 21%) – Melanoma (4 – 16%) – Colorectal tumors (2 – 12%) – Renal cell carcinoma (1 – 8%) – Lymphoma (< 10%) – Unknown origin (1 – 18%) Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p

31 Brain Tumors

32 Brain Tumor

33 Brain Tumors Headache Seizure Progressive focal neurological deficits Visual defects Altered mental status Intracerebral hemorrhage Intracranial pressure elevation

34 Hydrocephalus Caused by impaired cerebrospinal fluid flow, reabsorption or excessive production Cerebrospinal fluid – Forms at 0.3mL/min 20mL/hr 500mL/day – Total volume ~150mL 75mL in cranial vault – Normal pressure ~10mmHg Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p

35 Hydrocephalus

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37 Neuromuscular Disorders Acute generalized weakness – CNS Bilateral hemispheric Brainstem Spinal cord – Motor neuron West Nile infection Poliomyelitis Enterovirus infection – Neuromuscular junction Myasthenia gravis Lambert-Eaton myasthenic syndrome Organophosphate poisoning Botulism Tick Paralysis Hypermagnesemia Snake/insect/marine toxins Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 478

38 Neuromuscular Disorders Acute generalized weakness causes cont. – Neuropathies Guillain – Barré syndromes Critical illness polyneuropathy Chronic idiopathic demyelinating polyneuropathy Toxic neuropathies Vasculitic neuropathy Porphyric neuropathy Diptheria Lymphoma Carcinomatous meningitis Acute uremic polyneuropathy Eosinophilia-myalgia syndrome Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 478

39 Neuromuscular Disorders Acute generalized weakness causes cont. – Myopathies Critical illness myopathy Dermatomyositis Polymyositis Periodic paralysis/hypokalemic myopathy Myotonic dystrophy Acid maltase deficiency Muscular dystrophies Mitochondrial myopathies Corticosteroid-induced myopathy Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 478

40 Neuromuscular Disorders Causes of acute respiratory muscle weakness – CNS Diseases of high cervical cord or medulla – Motor neuron disease – Neuromuscular junction Myasthenia gravis Lambert-Eaton myasthenic syndrome – Neuropathies Idiopathic bilateral phrenic nerve paresis Guillain-Barré syndrome (rare) Neuralgic amyotrophy Large artery vasculitis Multifocal motor neuropathy – Myopathies Acid maltase deficiency Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 478

41 Neuromuscular Disorders Causes of acute predominantly bulbar weakness – CNS Brainstem diseases Bilateral white matter diseases Syrinx – Motor neuron Amyotrophic lateral sclerosis Kennedy disease – Neuromuscular junction Myasthenic gravis Lambert-Eaton myasthenic syndrome Botulism – Neuropathies Guillan-Barré syndrome (rare) Carcinomatous meningitis Skull base tumor or metastases Miller-Fisher disease Sarcoidosis Basilar meningitis – Myopathies Dermatomyositis Polymyositis Oculopharyngeal muscular dystrophy Myotonic dystrophy Distal myopathy with vocal cord paralysis Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 479

42 Neuromuscular Disorders Acute failure of the autonomic nervous system – CNS Diseases affecting the hypothalamus, brainstem, medulla, high cervical cord R insular stroke – Neuromuscular junction Lambert-Eaton myasthenic syndrome Botulism – Neuropathies Diabetic autonomic neuropathy Amyloid neuropathy Guillain-Barré with predominant dysautonomia Paraneoplastic dysautonomia Connective tissue disorders – Sjogrens – Systemic lupus erythematosus – Infectious – Chagas – HIV – Leprosy – Diptheria Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 479

43 Neuromuscular Disorders Indications for ICU admission – Respiratory weakness FVC < 40ml/kg NIF < - 40 cmH 2 O > 30% decline in FVC or NIF in 24 hrs Signs of fatigue or dyspnea Significant neck flexor weakness or poor cough CXR – Infiltrates, atelectasis or pleural effusion – Dysphagia/inability to protect airway Increased aspiration risk Bulbar dysfunction/bilateral facial weakness Failed swallow evaluation – Autonomic instability Dysrhythmia Blood pressure lability Profound sensitivity to sedatives – Planned interventions Plasma exchange Frequent vital checks or intensive nursing care Rapid onset of symptoms (< 7 days) Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 480

44 Neuromuscular Disorders Intubation indications – Consider early intubation May reduce pulmonary complications – FVC < 20 mL/kg – NIF < - 30 cmH 2 O – PaO 2 50% in 24 hrs) on room air – Hypoventilation (PaCO 2 > 45) – Dysphagia Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 480

45 Neuromuscular disorders Extubation criteria – Pressure support of 5 with PEEP 5 for > 2hrs (prolonged SBT) – Some evidence for PS of 0 with PEEP of 5 or T- piece predicts more successful extubation – Successful secretion management Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 481

46 Status Epilepticus A seizure that persists a sufficient length of time or is repeated frequently enough to produce a fixed and enduring epileptic condition Historically, is defined by a seizure lasting 30 min and should be considered for seizures lasting 5 – 10 min Nonconvulsant status epilepticus should be considered with coma patients with unclear etiology – May occur in as many as 8 -34% of critically ill patients Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 489

47 Status Epilepticus Etiologies – Neurovascular – Tumor – CNS Infection – Inflammatory disease – Traumatic brain injury – Primary epilepsy – Hypoxia/ischemia – Drug/substance toxicity or withdrawl – Fever – Metabolic abnormalities Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 491

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49 Status Epilepticus Medical treatment – May require inducing a coma – Neuromuscular blockade Will not stop the seizure, only the motor manifestation Airway and ventilator management – May not be required for nonstatus seizure – Will be required for induced coma Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 499

50 Spinal Cord Injury Trauma is the most common cause – ~ 50% are motor vehicle related – 24% related to falls – 9% sports injury – 11% assault – > 50% involve the cervical spine Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 325

51 Spinal Cord Injury Diaphragm – Innervated by cervical spine segments C 3 – C 5 Injury at or above this level results in immediate ventilatory failure – Below the diaphragmatic level Diaphragm is preserved Intercostals are compromised Decreased vital capacity, maximal inspiratory support and decreased expiratory force Spasticity develops leading to improved forced vital capacity and maximal expiratory force Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 333

52 Spinal Cord Injury Post injury – Rapid shallow breathing transiently compensates for the injury – Atelectasis develops – 1/3 will require intubation – Consider intubation when VC < 1L – Intubate if decreased LOC, impaired cough or unable to manage secretions Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 333

53 Neurogenic Pulmonary Edema Occurs in with severe acute neurological injury Incidence – 40% of head injury patients – 90% intracerebral hemorrhage

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55 Neurological evaluation

56 Neurological Evaluation Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 313

57 Physiological Effects of Neurological Injury Cerebral Blood Flow – Controlled by the arteriole constriction and relaxation Hypoventilation – Hypercarbia – Hypoxia

58 Autoregulation metrohealthanesthesia.com

59 Cerebral Perfusion Pressure (CPP) CPP = Mean arterial pressure (MAP) – Intracranial pressure (ICP)/Central venous pressure (CVP)

60 Monro-Kellie Doctrine

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62 Hyperventilation P a CO 2 – 1 mmHg change in P a CO 2 produces 1 ml/100 Gm/min change in CBF (in same direction) Transient effect (wanes in 6-8 hours) Normal CBF – PaCO2 = 40 mmHg

63 Management ABC – Airway GCS < 8 or rapid worsening GCS Uncontrolled seizures – Intubation Controlled induction – Avoiding hypo or hypertension – Consider lidocaine to blunt elevation in ICP Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p 357

64 Management ABC – Breathing Higher mortality rate in neurological patients than nonneurologic patients despite a lower incidence of extracerebral organ dysfunction Avoiding secondary injury – Lung Protective Ventilation – Circulation Target CPP 60 – 80 mmHg – ICP monitoring Necessary to accurately measure CPP Pelosi, et. al. Crit Care Med 2011 Vol. 39, No. 6

65 Ventilator management Mode PEEP Oxygenation – O 2 saturation > 90% – PaO 2 > 60 mmHg ARDS – Lung protective ventilation Neurogenic pulmonary edema Bullock, R, M.D., Ph.D., Deputy Editor, Povlishock, J., Ph.D. Editor-in-ChiefGuidelines for the Management of Severe Traumatic Brain Injury of Severe Traumatic Brain Injury 3rd ed, 2007 Brain Trauma Foundation, Inc.

66 PEEP – Increases Intrathoracic pressure Peak inspiratory pressure Mean airway pressure – Decreases Venous return Mean arterial pressure Cardiac output

67 PEEP PEEP 5 – 15 mmHg – Generally tolerated in patients at risk for elevated ICP – Elevated ICP should be closely monitored with changes in PEEP

68 Venous Drainage

69 Extubation Neurosurgical patient – GCS = 4 were successfully extubated Intact cough and gag – Strategy Is the neurological injury reversible? What is the duration of injury? – If long term neurological injury anticipated Early tracheostomy

70 Extubation Criteria – Signs of appropriate muscle strength – Vital capacity > 15 – 20 mL/kg – Mean inspiratory pressure < -20 to -50 cmH 2 O – FiO 2 < 40% and PEEP ≥ 5 cmH 2 O – No fever, infection or other medical complications

71 Pulmonary toilet Endotracheal suctioning on cerebral oxygenation in traumatic brain-injured patients – Increased ICP – Increased CPP – No change in oxygenation Kerr, et al, Critical Care Medicine, Volume 27(12), December 1999, pp

72 Monitors ICP Monitors – Bolt Pressure monitor – External Ventricular Drain (EVD) Pressure monitor Drainage of CSF – Parenchymal ICP monitor (Codman) Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p

73 Tissue oxygenation – Jugular venous saturation – Brain tissue oxygenation (Licox) – Near – infrared spectroscopy Tissue metabolic activity – Microdialysis catheter Monitors Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2nd ed. Springer, 2011, p

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75 Summary Recognition of neurological injury ABCs Intubation and Ventilation Extubation

76 References 1.Bhardway, Anish, et. al., ed, Handbook of Neurocritical Care, 2 nd ed. Springer, 2011.


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