Respiratory disease main cause of death in Spinal Cord Injury

1. Respiratory disease main cause of death in Spinal Cord Injury

2. A & P Refresher • Acute phase • Respiratory • Cardiovascular • Chronic phase • Respiratory • Cardiovascular

3. 68 patients >C5 88% needed intubating C5-C8 60% needed intubating Velmahos gc et al American surgeon 2003 156 Patients Injuries C2-C8 107 required tracheostomies Harop et al Journal of neurosurgery spine 2004 Respiratory compromise Level of injury Age Premorbid resp. disease

4. MAG (myelin-associated glycoprotein), Omgp (oligodendrocyte myelin glycoprotein), KDI (synthetic: Lysine–Asparagine–Isoleucine ‘g-1 of Laminin Kainat Domain’), Nogo (Neurite outgrowth inhibitor), NgR (Nogo protein Receptor), the Rho signaling pathway (superfamily of ‘Rho-dopsin gene including neurotransmitter receptors‘), EphA4 (Ephrine), GFAP (Glial Fibrillary Acidic Protein), different subtypes of serotonergic and glutamatergic receptors, antigens, antibodies, immune modulators, adhesion molecules, scavengers, neurotrophic factors, enzymes, hormones, collagen scar inhibitors, remyelinating agents and neurogenetic/plasticity inducers Pathophysiology Trauma ↓ Haemorrhage/Inflammatory mediators ↓ Oedema ↓ Ischaemia ↓ Oedema ↓ Ischaemia ↓ Oedema ↓ Ischaemia ↓

6. Cardiorespiratory physiology

8. Respiratory Afferents Intrapulmonary receptors Vagus Stretch/proprioreceptors ribs/intercostals T1-T12 Clavicles Low Cervical Chemoreceptors Carotid body Chemoreceptors Brainstem

9. Acute changes Damaged cord becomes unresponsive Flaccid, areflexic Lasts for 6 days to 6 weeks

10. Respiratory • Can’t breath • Can’t cough

11. Acute VC 1 Year VC Lumbar Unable to cough 100-70% 100-70% Low thoracic é chest wall compliance ê Vital capacity High thoracic éé chest wall compliance 30-50% êê Vital capacity poor expansion. Basal collapse 60-70% C5/C6 Diaphragms, Scalenes, 20% 40-50% C3/C4/C5 Sternomastoid and partial diaphragm Above C3 Sternomastoid only 5-10%

13. Acute changes respiratory autonomic Bronchial hypersecretion Bronchial hyper-responsiveness

14. Not forgetting… Head injuries Chest wall trauma Pulmonary contusion Haemopneumothorax PE/ Fat embolus

15. Acute Respiratory monitoring Lung function FVC, PEFR, Speech, RR, Resp Pattern FVC> 1L FVC < 1L FVC= Tidal volume Pulse oximeter Blood gasses Watch closely in an appropriate environment for several days Aspiration risk

16. Acute respiratory treatment Oxygen A good physiotherapist ! NIPPB (Birding) Non-invasive ventilation Invasive ventilation Tracheostomy

17. Secretion management • Carbocysteine • N acetylcysteine nebs • ? Saline nebs ? • Bronchodilator nebs • ? Hyoscine? • Azithromycin/ colistin nebs for colonisation • Supraglottic suction tubes

18. Cardiovascular • Can’t squeeze • Can’t speed up

19. Parasympathetic Sympathetic Parasympathetic  Vasoconstriction Vasodilation T6 Balance point Hypotension, bradycardia, tendency to asystole

20. Acute changes cardiac Be carefull….. Neurogenic pulmonary oedema Postural hypotension Vagal stimulation (tracheal suction) Pressure sores

21. Aim to maintain adequate perfusion Vale et al, Journal of neurosurgery aug 1997 Combined medical and surgical treatment after acute spinal cord injury: results of a prospective study To assess the merits of aggressive medical resuscitation and blood pressure management Hypotension Bradycardia (Pacemakers) How high? How long?

22. Other common problems… • Nutrition and GI tract • Renal function • Temperature control • Psycological • DVT • 30% incidence • Documentation • Pain

23. Chronic changes • Spontaneous function returns • Lack of descending inhibition • Augmentation of cross spinal reflexes • Enhanced reflex sensitivity • Spasms and spasticity

24. Chronic changes respiratory VC Improves Cough improves Secretions lessen Long term ? Sleep disordered breathing

25. Chronic changes cardiac Postural hypotension stays Vagal hypersensitivity fades Bradycardia remains

26. Chronic changes cardiac Autonomic dysreflexia Autonomic hyperreflexia Sympathetic discharge due to autonomic stimulus T6 and above Peripheral and central vasoconstriction below injury level Compensatory vasodilatation above injury level Severe hypertension, headache, Bradycardia Sweating above injury level Asystole, myocardial infarction, cerebral haemmorhage

27. Chronic changes cardiac Autonomic dysrefflexia Triggered by………. Bladder distension Bowel distension Minor infections Major infections Treat by……….. Remove cause Nifedipine GTN

28. Hospitalised 1 year mortality 15% National Spinal Cord Injury Statistical Centre, University of Alabama