EXAM 3 REVIEW Flashcards
C5
ELBOW FLEXORS
C6
WRIST EXTENSORS
C7
ELBOW EXTENSORS
C8
FINGER FLEXORS
T1
FINGER ABDUCTORS (LITTLE FINGER)
L2
HIP FLEXORS
L3
KNEE EXTENSORS
L4
ANKLE DORSIFLEXORS
L5
LONG TOE EXTENSORS
S1
ANKLE PLANTAR FLEXORS
How long does spinal shock last (hemodynamic disturbances)
1-3 weeks
Reduction in BP after acute spinal cord injury due to
Loss of sympathetic tone and decreased SVR
Bradycardia from loss of T1-T4 innervation of the heart
Complications 2 years after INJURY in order of from most incidence to least incidence (USCD A-SHPRP)
UTI (59%) Skeletal muscle spasticity (38%) Chills and fever (19%) Decubitus ulcer (16%) Autonomic hyperreflexia (8%) Skeletal muscle contractures (6%) Heterotopic ossicification(3%) PNA (3%) Renal dysfunction (2%) Postop wound infection (2%)
Complications 30 years after INJURY in order of from most incidence to least incidence (DSGC UI-VUMR)
Decubitus ulcer (17%) Skeletal muscle or joint pain (16%) GI dysfunction (14%) CV dysfunction (14%) UTI (14%) ID or Cancer (11%) Visual or hearing disorders (10%) Urinary retention (8%) Male GU dysfunction (7%) Renal Calculi (6%)
Several weeks after acute spinal cord injury, spinal cord reflexes
gradually return, and patients enter a chronic stage
After several weeks after Acute SCI patient enters a chronic stage characterized by
characterized by overactivity of the sympathetic nervous system and involuntary skeletal muscle spasms
Injury at or above C5 =
apnea due to denervation of the diaphragm
Succinylcholine is likely to provoke hyperkalemia
within the
first 6 months after injury (Avoid it after 24 hours of injury)
When does Autonomic hyperreflexia appear?
Appears AFTER spinal shock in association with
return of spinal cord reflexes
Autonomic Hyperreflexia Can be initiated by
cutaneous or visceral stimulation below the level of spinal injury
Autonomic hyperreflexia common stimuli
Surgery or distention of hollow viscus (bladder, rectum) are common stimuli
Autonomic hyperreflexia Stimulation does what? then end result is ?
initiates afferent impulses that enter the spine, this elicits an increase in sympathetic nervous system activity along the splanchnic outflow tract (in normal patients, this is inhibited by higher centers of the CNS) . End result is a Generalized systemic vasoconstriction occurs BELOW the level of the spinal cord injury
Generalized systemic vasoconstriction occur
BELOW the level of the spinal cord injury
Autonomic hyperreflexia patho
- Stimulus below level of spinal cord transection
- Activation of preganglionic sympathetic nerves
- Vasoconstriction
- Hypertension
- Carotid sinus
- Vasodilation /Bradycardia
- Activation of pre-ganglionic sympathetic nerves
What is the hallmark of autonomic hyperreflexia?
Hypertension and REFLEX BRADYCARIDIA (carotid sinus stimulation)
When there is reflex cutaneous vasodilation ?
Reflex cutaneous vasodilation ABOVE the level of spinal injury (nasal stuffiness)
Autonomic Hyperreflexia Neuro symptoms
Headache, blurred vision = severe hypertension (can lead to LV failure)
Who experienced and DO not experience autonomic hyperreflexia?
85% of patients with lesions above T6 exhibit this reflex, unlikely to be associated below T10
Splanchnic nerve and innervations: GREATER SPLANCHNIC NERVE
T5-T9
Splanchnic nerve and innervations: LESSER SPLANCHNIC NERVE
T10-T11
Splanchnic nerve and innervations: LEAST SPLANCHNIC NERVE
T12
Loss of input from higher centers to these nerves
increase risk of exaggerated autonomic reflexes
T5-T12
***Management for exaggerated autonomic reflexes
prevent it! Have vasodilators available (SNP, hydralazine), can occur in PACU when drugs begin to wear off
Loss of input from higher centers to nerve T5-T9, T10-T11 and T12 leads to
Increase risk of exaggerated autonomic reflexes
what happens to the parts of the body ABOVE the level of the spinal cord lesion
VASODILATATION
When GA is selected, avoid
Succinylcholine 24 hours after injury due to risk of hyperkalemia. use NDNMB agents
Autonomic Hyperreflexia occurs in patients with spinal cord injury what level
Above T6
CREST Syndrome
Calcinosis: Calcium deposits in the skin
Raynaud’s Phenomenon: Spasm of blood vessels with
cold or stress.
Esophageal dysfunction: Acid reflux and decrease
esophageal motility.
Sclerodactyly: Thickening and tightening of the skin on
fingers and hands.
Telangiectasias: Dilation of capillaries causing red
marks on skin surface
3 main problems with MARFAN (HPK)
High Arched palare
Pectus excavatum (spoon chest)
Kyphoscoliosis
Marfan’s syndrome most deaths caused by
Cardiovascular
Most common cause of
Mitral Prolapse
Mitral Regurgitation
Mitral stenosis
Snap
MVP
Mid systolic click late systolic murmur
Aortic issue with Marfan
Aortic dilation
Aortic dissection or rupture
Issue with Marfan and CT
Defective CT in aorta and heart valves.
Cardiac Conduction abnormality with Marfan is
BBB common
Respiratory with Marfan 2 common developments
Early development of emphysema
High incidence of spontaneous pneumothorax
Marfan’s Syndrome Anesthesia Considerations
Mainly focus on ?
CV Focus on cardiopulmonary abnormalities
Marfan’s syndrome patients and AIRWAY
Susceptible to temporomandibular joint dislocation
→caution with jaw thrusting
Marfan syndrome and BP considerations
AVOID any sustained increase in systemic blood pressure r/t increased risk of aortic dissection
Marfan and monitoring
Invasive monitoring including TEE consideration in selected patients
High risk for the development of pneumothorax
What kind of patients –>
Marfan’s syndrome
FORMAL DIAGNOSIS of ARF
• INCREASED SERUM CREATININE MORE THAN 0.5 MG/DL OF BASELINE
• 50% DECREASE IN CREATININE CLEARANCE
• A CHANGE IN SERUM CREATININE OF GREATER THAN 0.3 MG/DL WITHIN 48 HOURS OF
ACUTE INSULT
RENAL BLOOD FLOW (RBF) (AUTOREGULATED @
50 TO 150 MMHG
Most susceptible cause ➔
RENAL TUBULE ISCHEMIA (MOST SUSCEPTIBLE) ➔ PROLONGED ➔ IRREVERSIBLE CORTICAL NECROSIS.
Chronic Renal Failure
HYPERKALEMIA, HYPERMAGNESEMIA, HYPERPHOSPHATEMIA, HYPOCALCEMIA
CRF METABOLIC ACIDOSIS -ANEMIA
INCREASED CO, RIGHT SHIFT OF OXYHEMOGLOBIN DISSOCIATION CURVE
Lumbar lordosis/kyphoscoliosis and neuraxial
⇧neuraxial technical difficulty and positioning concerns
EHLERS – DANLOS SYNDROME and neuraxial
Bleeding: Avoid IM injections; excessive instrumentation of nose or esophagus; laryngoscopy; A line or CVP (hematoma);
no regional anesthesia (too much bleeding)
Achondroplasia Dwarfism, Small epidural space =
difficult to introduce epidural catheter
Osteophytes, prolapsed intervertebral discs, or deformed vertebral bodies also contribute to difficulties with neuraxial blockade
Duschenne Muscular Dystrophy and Regional anesthesia
avoids the unique risks of general anesthesia in Duschenne Muscular Dystrophy.
Nemaline Rod Muscular dystrophy Regional anesthesia
high motor block could = respiratory compromise
Myotonic dystrophy:
GA, regional and NMB do NOT prevent/relieve contraction
High concentrations of VA may
decrease contractions but will also cause myocardial depression
What is Nemaline Rod Muscular Dystrophy is a
Slowly progressive symmetrical dystrophy of skeletal and smooth muscles.
Nemaline Rod Muscular Dystrophy and motor
Delayed motor development; muscle weakness; hypotonia, abnormal gait, and loss of deep tendon reflexes
Nemaline Rod Muscular Dystrophy Facial
Micrognathia, dental malocclusion
Nemaline Rod Muscular Dystrophy Skeletal abnormalities
Kyphoscoliosis and pectus excavatum
Heart and Nemaline Rod Muscular Dystrophy
Dilated cardiomyopathy ➔ cardiac failure.
Nemaline Rod Muscular Dystrophy NEURO
Normal mentation
Nemaline Rod Muscular Dystrophy Anesthesia Consideration : INTUBATION
- Difficult tracheal intubation due to micrognathia and high arched palate
- Awake fiberoptic endotracheal intubation may be needed
Nemaline Rod Anesthesia Consideration Respiratory
Respiratory depressant effects of drugs may be exaggerated d/t respiratory muscle weakness and chest wall abnormalities
Nemaline Rod Anesthesia Considerations: Ventilation
V/Q mismatch increased; ventilatory response to CO2 may be blunted
Nemaline Rod Anesthesia Considerations: MUSCLE RELAXANTS
Sux and NDNMB response is unpredictable
Not been reported with Nemaline Rod
MH
What is Periodic Paralysis?
Intermittent acute attacks to skeletal muscle ➔ weakness or paralysis
Causes of Periodic Paralysis
hypo or hyperkalemia
Anesthesia Considerations for PERIODIC PARALYSIS 2 meds
- Acetazolamide
2. Mannitol
Monitor this and AVOID 2 meds in Periodic Paralysis
Frequent K+ monitoring
Avoid potassium solutions
Avoid succinylcholine
Treatment for Periodic Paralysis
Administer glucose containing solutions if treating hyperK c/insulin
Clinical Features of Familial Periodic Paralysis Type: HYPOKALEMIA K value
<3.0
Clinical Features of Familial Periodic Paralysis Type: HYPOKALEMIA : PRECIPITATING FACTORS
PAMGHHSS- CE
Pregnancy Anesthesia Menstruation Glucose infusion HIgh Carb meal Hypothermia Strenuous Exercise Stress
Cardiac Dysrhythmias
ECG signs of Hypokalemia
Clinical Features of Familial Periodic Paralysis Type: HYPERKALEMIA K value
> 5.5
Clinical Features of Familial Periodic Paralysis Type: HYPERKALEMIA : PRECIPITATING FACTORS
PHEM
Potassium Infusion
Hypothermia
Exercise
Metabolic Acidosis
Clinical Features of Familial Periodic Paralysis Type: HYPERKALEMIA: OTHER FEATURES
Skeletal muscle weakness may be localized to tongue and eyelids
MYASTHENIA GRAVIS - What is MG
Chronic autoimmune disorder caused by a decrease in functional acetylcholine receptors (AchR) at the NMJ resulting from destruction or inactivation by circulating antibodies
ACH receptor and MG
Down regulation of AchR
2/3 of patient with MG have
Thymic hyperplasia is present in two thirds of patients with myasthenia gravis, and 10% to 15% of these patients have thymomas
What is the Hallmark of MG:
weakness and rapid exhaustion of voluntary muscles with repetitive use
Partial recovery with rest; muscle strength is normal when well rested
MG Initial symptoms:
ptosis, diplopia, and dysphagia
MG and Aspiration
High aspiration risk (Weak pharyngeal, laryngeal muscles = dysphagia, dysarthria and difficulty handling saliva
MG and heart
Myocarditis can result in atrial fib, heart block, or cardiomyopathy
Other autoimmune diseases that may precipitate MG
HPRS
Hyperthyroidism
Pernicious anemia
Rheumatoid arthritis
Systemic lupus erythematosus
What are meds that can aggravate muscle weakness
Antibiotics, especially aminoglycosides, can aggravate muscle weakness
May precipitate or exacerbate muscle weakness in Myasthenia Gravis (PIESE)
Pregnancy Infection Electrolyte abnormalities, Surgery Emotional stress
Treatment of Myasthenia Gravis PIP-T
Pyridostigmine
Immunosuppressive Therapy
Plasmapheresis
Thymectomy
Anesthesia Considerations of Myasthenia GRAVIS
MUSCLE RELAXANTS
⇧ sensitivity to NDNMB; decrease dose by ½ to 2/3 Or just avoid it completely
Resistance to succinylcholine Need 2.6 X the ED95
MG and Volatile agents
VA have MS relaxation properties
Postpone extubation and ventilator support postop.
MYASTHENIC SYNDROME AKA Eaton-Lambert Syndrome
What is it?
Resembles Myasthenia Gravis IgG antibodies attack Ca2+ channels
Treatment of Myasthenic Syndrome
3,4 Diaminopyridine
• IgG (6 to 8 weeks).
Myasthenia syndrome Anesthesia Considerations
Sensitive to depolarizing and non-depolarizing NMB
Antagonism of NM-Blockade with anticholinesterase drugs may be inadequate.
The potential presence of myasthenic syndrome and the need to decrease doses of muscle relaxants should be
Considered when?
considered in patients undergoing bronchoscopy, mediastinoscopy, or thoracoscopy***for suspected lung cancer
Epidermolysis Bullosa Despite
dystrophic skeletal muscle, no increased risk of a hyperkalemic response when treated with succinylcholine
Scleroderma Musculoskeletal system:
myopathy- weak, mostly proximal skeletal muscle groups
EHLER”S DANLOS SYNDROME Musculoskeletal: Joint
hypermobility, musculoskeletal discomfort, susceptibility to osteoarthritis.
DERMATOMYOSIS
Abnormal immune responses ➔ Slow, progressive skeletal muscle damage
S/ S of Dermatomyosis S
keletal muscle weakness (e.g., difficulty climbing stairs) d/t skeletal muscle destruction ➔ increased serum creatine kinase levels.Neuromuscular junction is not affected
Neuromuscular junction is not affected
Dermatomyosis
Marfan’s Syndrome Additional skeletal abnormalities
PKHH
Pectus excavatum
Kyphoscoliosis
Hyperextensibility of the joints
High-arched palate
Duschenne Muscular dystrophy Group of
hereditary diseases characterized by painless degeneration and atrophy of skeletal muscles
Duschenne Muscular Dystrophy
Progressive, symmetrical skeletal muscle weakness and wasting but no evidence of skeletal muscle denervation
Initial symptoms of Duschenne Muscular Dystrophy
waddling gait, frequent falling, difficulty climbing stairs, and these reflect involvement of the proximal skeletal muscle groups of the pelvic girdle
Affected muscles become larger as a result of fatty infiltration
Duschenne Muscular dystrophy and ambulation
Predispose to ?
Typically confined to a wheelchair by age 8 to 10
Skeletal muscle atrophy can predispose to long bone fractures
PRADER WILLI SYNDROME and skeletal
Weak skeletal musculature = poor cough and ⇧pneumonia
Systemic Lupus Erythematous *(SLE) is a
Multisystem chronic inflammatory disease characterized by antinuclear antibody production
SLE exacerbated by
Exacerbated by infection, pregnancy, surgery
SLE Onset can be drug induced: PHIDA
Procainamide hydralazine Isoniazide, D - penicillamine ALpha - methyldopa
Treatment of SLE (CIB)
Corticosteroids
Immunosuppressive treatment
Bone marrow transplant
Anesthesia Considerations for SLE
CRML
Laryngeal involvement
Mucosal ulceration
Cricoarytenoid arthritis
Recurrent laryngeal nerve palsy, may be present in as many as 1/3 patients
Periodic Paralysis: Avoid
Potassium solutions
Periodic Paralysis: CAUSES
HYPO and HYPERKALEMIA
Epidermolysis Bullosa and K+ and SUCC
NO INCREASED OF HYPERKALEMIC RESPONSE WITH SUX
Duschenne Muscular dystrophy Succinylcholine
contraindicated d/t risk of rhabdomyolysis, hyperkalemia, and/or cardiac arrest -
Duschenne Muscular dystrophy: VA
Rhabdomyolysis, with or without cardiac arrest, observed with administration of VOLATILE anesthetics to these patients even in the absence of succinylcholine
What is Mastocytosis
Rare; disorder of mast cell proliferation; degranulation of mast cells
Mastocytosis Urticaria pigmentosa is usually
benign and asymptomatic
Children are most often affected → resolves by adulthood
Systemic mastocytosis : What happens
mast cells proliferate in all organs (especially bone, liver, and spleen, but not in the CNS).
Signs and Symptoms of Mastocytosis
Histamine release from mast cells and prostaglandins are involved➔ anaphylactoid responses characterized by pruritus, urticaria, and flushing with hypotension (life threatening) and tachycardia
Mastocytosis and bronchospasm,
Low risk of bronchospasm Bleeding unusual, even though mast cells contain heparin!
Anesthetics Management for MASTOCYTOSIS Influenced by
the possibility of intraoperative mast cell degranulation and anaphylactoid reaction
-Have epinephrine readily available
Mastocytosis : Contrast dye
has caused profound hypotension- pretreat with H1,H2 blockers and glucocorticoid
Mastocytosis and Cromolyn-
inhibits mast cell degranulation, i.e. release of histamine (also used to treat asthma) -
Mastocytosis Safe: VVPF
Volatile anesthetics,
Vecuronium.
Propofol
Fentanyl
Mastocytosis Avoid:
Succinylcholine and Meperidine may cause mast cell degranulation
Upper cervical spine most at risk
(C1-C3)
Morbidity and mortality for cervical injuries include
alveolar hypoventilation with inability to clear bronchial secretions, plus the risk of aspiration of gastric contents, pneumonia, and pulmonary embolism (slide 5)
Lateral protrusion of a cervical disk usually occurs at
C5-6 or C6-7 intervertebral spaces
Symptoms can be exaggerated by coughing
CERVICAL INJURY Management of anesthesia: primary concern is
airway approach, direct laryngoscopy should only be done if no significant worsening of symptoms occur with neck movement (especially extension)
Management of anesthesia: cervical spine procedures via the anterior approach
involves retraction of the airway structures and may result in injury to the ipsilateral recurrent laryngeal nerve and can manifest as hoarseness, stridor, or frank airway compromise
MANAGEMENT OF CERVICAL SPINE PROCEDURES Compression of
Recurrent laryngeal nerve fibers can be caused by the endotracheal tube or the inflated cuff. It is common practice to decrease the cuff completely and reinflate it until a leak is no longer heard
Cervical spondylosis =
neck pain and radicular pain in the arms and shoulders accompanied by sensory loss and skeletal muscle wasting. Later, sensory and motor signs may appear in the legs producing an unsteady gait
UNSTABLE C-NECK
Sensitivity of plain radiographs for detecting cervical spine _____THEREFORE
injury is < 100%, treat all acute cervical spine injuries as potentially unstable
Immediate immobilization to limit
neck flexion/extension
Manual in-line stabilization during laryngoscopy
CERVICAL SPINE movement tend to
Movement tends to occur in the occipito-atlanto-axial area even with stabilization
Neck hyperextension can further
damage the spinal cord
Anesthetic implications for old spinal injury. Chronic spinal cord injuries lead to ICACAA
Impaired alveolar ventilation Cardiovascular instability Autonomic hyperreflexia), Chronic pulmonary and genitourinary tract infections, Anemia Altered thermoregulation
Chronic spinal cord injuries and renal
Renal failure can occur
Anesthetic implications for old spinal injury.Immobility leads to
osteoporosis, skeletal muscle atrophy, DVT/VTE, pathologic fractures
Several weeks after acute spinal cord injury,
spinal cord reflexes gradually return, and patients enter a chronic stage characterized by overactivity of the sympathetic nervous system and involuntary skeletal muscle spasms
Spasm with spinal cord injury Medication to help and how it works
Baclofen
potentiates GABA) is useful to treat spasticity (abrupt withdrawal = seizures
Chronic Spinal Cord Injury
Injury at or above C5 there is ______Due to
apnea due to denervation of the diaphragm
Even when the diaphragm is intact, coughing and the ability to clear secretions from airway may be impaired due to denervation of intercostal and abdominal muscles
Injury at or above C5 RESPIRATORY CHANGES
What does anesthetist need to do? What can occur?
Marked decreased vital capacity, arterial hypoxemia Need to preoxygenate before suctioning (bradycardia or cardiac arrest can occur)
Chronic Spinal Cord Injury Management of Anesthesia
Prevent autonomic hyperreflexia
Chronic Spinal Cord Injury Management of Anesthesia; Muscle Relaxant
Use NDNMB to prevent reflex skeletal muscle spasms in response to surgical stimulation
Chronic Spinal Cord Injury Management of Anesthesia: SUCC
Succinylcholine is likely to provoke hyperkalemia within the first 6 months after injury (Avoid it after 24 hours of injury)
Chronic Spinal Cord Injury Management of Anesthesia: ANTICIPATE what? What medication not to stop ?
Anticipate altered hemodynamics
Continue Baclofen and benzodiazepines perioperatively
What is Amyotrophic Lateral Sclerosis (ALS)
Degenerative disease involving the lower motor neurons in the anterior horn gray matter of the spinal cord and the corticospinal tracts (primary descending upper motor neurons)
ALS produces
Produces both upper and lower motor neuron degeneration
Most common affected with ALS
Most commonly affects men 40-60 years of age
ALS: Primary lateral sclerosis
= limited to the motor cortex of the brain
ALS Pseudobulbar palsy =
limitation to the brainstem nuclei
Amyotrophic Lateral Sclerosis Symptoms reflect and resemble what?
upper and lower motor neuron dysfunction (resembles myasthenia gravis)
ALS Begins with
Skeletal muscle atrophy
Weakness
Fasciculations in the hands
Eventually includes all skeletal muscles including the tongue, pharynx, larynx, and chest TPLC
ALS Bulbar involvement includes
fasciculations of the tongue plus dysphagia, which leads to pulmonary aspiration
With ALS Autonomic nervous system dysfunction can be manifested as
Orthostatic hypotension and resting tachycardia
Muscles Spared with ALS
Ocular muscles are spared
Amyotrophic Lateral Sclerosis Anesthesia considerations: RESPIRATORY
Exaggerated respiratory depression
Amyotrophic Lateral Sclerosis Anesthesia considerations
Vulnerable to
Vulnerable to hyperkalemia following succinylcholine administration
Amyotrophic Lateral Sclerosis Anesthesia considerations NDNMB
Prolonged responses to NDNMBA
What predisposes ALS patients to aspiration
Bulbar involvement predisposes to pulmonary aspiration
Syringomyelia (syrinx) is a disorder where there is
cystic cavitation of the spinal cord
Syringomyelia (syrinx) What is called syringobulbia?
Rostral extension into the brainstem
Syringomyelia (syrinx) - Communicating syringomyelia =
Either only dilation of the central canal of the cord (hydromyelia) or there is communication between the abnormal cystic lesions in the spinal cord proper and the CSF spaces
Syringomyelia - What is communicating syringomyelia associated with?
Associated with basilar arachnoiditis or Chiari’s malformation
Syringomyelia- Noncommunicating syringomyelia =
presence of cysts that have no connection to the CSF spaces
Syringomyelia Symptoms:
sensory impairment involving pain and temperature sensation in the upper extremities (destruction of neuronal pathways), as cavitation progresses, destruction of lower motor neurons ensues causing skeletal muscle weakness and wasting and loss of reflexes
Syringomyelia Thoracic scoliosis why?
Thoracic scoliosis can result from weakness of paravertebral muscles
Syringobulbia
paralysis of the palate, tongue, and vocal cords
Syringomyelia Management of anesthesia:
TEAT
Thoracic scoliosis can cause V/Q mismatching
Avoid succinylcholine due to lower motor neuron disease
Exaggerated responses to nondepolarizing muscle relaxants
Thermal regulation may be impaired
GFR
best measure of renal function • normal: > 90 ml/min
Creatinine clearance •
Most reliable measure of GFR
Normal CrCL
110-140ml/min
Serum creatinine
Normal: 0.6 to 1.3 mg/dl
Blood urea nitrogen (bun) • normal:
10 to 20 mg/dl
Function of Renal system
Sodium and water removal
Waste removal
Hormone production
Kidney Filter the plasma volume every
22 minutes
3 things kidney regulate OVP
- Regulation of plasma osmolarity
- Regulaiton of plasma volume
- Regulation of arterial pH (acid-base)
3 things kidney regulate OVP
Regulation of plasma osmolarity
Regulaiton of plasma volume
Regulation of arterial pH (acid-base)
Kidney Removal of
metabolic water and foreign substances (urea and drugs)
Kidney produces and activation of
Production of erythropoietin and renin
Actionvation of Vitamin D 3
Fluid overload problems in kidneys
Elevated wastes products (Urea, creatinine, potassium)
Changes in hormone control in the kidney (BUM)
Blood pressure
Making RBCs
Uptake of calcium
Filtration is
movement of fluid from glomerulus to Bowman’s capsule
Tubular Reabsorption is
Movement from Bowman’s capsule to Peritubular capillaries
Tubular Secretion is
Movement from Peritubular capillaries to Bowman’s capsule
Proximal tubule NaGluKAHPPUH
reabsorption of NaCL Glucose K Amino Acids HCO3 PO4 Protein Ureak H2O ( ADH not required)
Tonicity of fluid (within ducts) Proximal
Isotonic
Tonicity of fluid (within ducts) Loop of Henle
Isotonic, Hypertonic, Hypotonic
Tonicity of fluid (within ducts) Distal
Isotonic or Hypotonic
Tonicity of fluid (within ducts) Collecting duct
Final Concentration
Proximal tubule Secretion of (HFOI)
H+
Foreign Substances
Organic Anions, Catiion
Isotonic
Where is ADH not required
Proximal
LOOP of HENLE (CADU)
Concentration of urine (countercurrent mechanism)
Ascending loop Na+ Reabsorbed (active transport, water stays in)
Descending loop WATER Reabsorbed Nacl diffuses in
Urea secretion in thin segment
Distal Tubule NHH
KUHNS
Reabsorption of NaCL, H2O (ADH required) HCO3 Secretion of KUHNS K+ Urea H+ NH3+ Some drugs
Distal Tubule NHH KUHNSI
Reabsorption of NaCL, H2O (ADH required) HCO3 Secretion of KUHNSI K+ Urea H+ NH3+ Some drugs Iso or Hypo
Connecting Tubule Reabsorption of
H2O (ADH required)
COLLECTING Reabsoprtion OR secretion of NaKHN
Na+
K+
H+
NH3+
COLLECTING DUCT urea secretion in
Medulla
Major sites of exchange within the nephron: Reabsorption in Proximal (NHG)
Na+
H2O
Glucose
Major sites of exchange within the nephron: Reabsorption in Distal Tubule ()
H2O and K+
Secretion NH3
Major sites of exchange within the nephron: Secretion in Distal tubule
NH3
H+
ACUTE RENAL FAILURE (ARF)
• PERIOPERATIVE ANESTHESIA CONSIDERATIONS
Fluids
- NS VS. LR
• NS ➔ HYPERCHLOREMIC METABOLIC ACIDOSIS ➔ SECONDARY HYPERKALEMIA.
Acure Renal Failure, action of ALPHA 1 AGONIST VS. VASOPRESSIN
increased systemic pressure is accompanied by reduced renal sympathetic tone and vasodilation
ARF Alpha 1 agonist vs vasopressin
Alpha 1 agonist: ARF r/t sepsis with renal vasoconstriction ➔ exacerbate tubular injury. • • alpha 1 agonist: arf r/t sepsis with renal vasoconstriction ➔ exacerbate tubular injury. • vasopressin: selectively constrict renal efferent arterioles ➔ preserve gfr and uop.
Vasopression is better than alpha 1 agonist why?
vasopressin: selectively constrict renal efferent arterioles ➔ preserve GFR and Urine OUTPUT
CRF perioperative anesthesia considerations IV access:
use temporary hemodialysis catheter (not encouraged) ➔ must be accessed aseptically. • a line: not in same extremity as patent fistula ➔inaccurate arterial pressure and abg concentrations.
CRF induction ➔
hypovolemia ➔ impaired peripheral vasoconstriction. • give 250ml of 5% albumin via direct ivp using a 60ml syringe before induction.
In CRF, Giving Albumin, How does it help?
this “somewhat” corrects hypoalbuminemia, giving protein bound drugs something to bind to. it also acts as a volume expander helping to decrease hypotension’
RENAL TRANSPLANTATION
• ANESTHESIA CONSIDERATIONS: Fluid and volume
A high-normal systemic blood pressure and euvolemia are required to maintain adequate urine output
RENAL TRANSPLANTATION
• ANESTHESIA CONSIDERATIONS: VENTILATION
surgical retraction in the area of the diaphragm ➔ respiratory mechanics impaired ➔ *** controlled mechanical ventilation preferred •
Renal transplant: Old kidney vs new kidney clearance
A newly transplanted kidney can clear neuromuscular blockers and anticholinesterase drugs at the same rate as a healthy native kidneys
Monitoring and Meds after kidney transplant
Cvp monitoring should be used to guide volume infusion
Mannitol is administered to facilitate urine formation in the new kidney and decrease the risk of acute tubular necrosis
RENAL TRANSPLANTATION
• RELEASE OF VASCULAR CLAMPS ➔
➔ venous drainage from the legs and preservative solutions from the transplanted kidneys are released into circulation ➔ cardiac arrest can occur during this time due to hyperkalemia (potassium-rich preservative solutions)
2 reasons Why Hypotension after unclamping during renal transplantation?
➔ hypotension can follow unclamping because
- there is a 300 ml increase to the intravascular capacity
- previously ischemic tissues release vasodilating metabolic byproducts.
Anesthesia considerations for someone who has had a kidney transplant: • immunosuppressant drugs have multiple side-effects What are they (SLAT)
Systemic hypertension
Lowered seizure thresholds
Anemia
Thrombocytopenia
Anesthesia considerations for someone who has had a kidney transplant GFR and RBF.
GFR and renal blood flow likely to be lower, activity of drugs excreted by the kidneys may be prolonged •
Anesthesia considerations for someone who has had a kidney transplant Minimize
minimize drugs that depend on renal clearance, avoid nephrotoxins
When should diuretics be administered for someone who has had a kidney transplant
diuretics should only be administered after careful evaluation of intravascular volume status • decreases in renal blood flow should be minimized
Nephrotic syndrome • definition:
daily urinary protein excretion exceeding 3.5 g
Nephrotic syndrome associated with (SHIT)
Sodium retention
Hyperlipidemia,
Infectious complications
Thromboembolic
Nephrotic syndrome most common cause:
diabetic nephropathy •
Nephrotic syndrome signs and symptoms • revolve around
Sodium retention and decreased plasma oncotic pressure leading to intravascular hypovolemia and edema
Signs of Nephrotic syndrome (VOPT)
Vasoconstriction
Orthostatic hypotension
Peripheral
Tachycardia,
To correct hypovolemia with Nephrotic Syndrome
Infusion of albumin to correct hypovolemia,
Loop diuretics and Nephrotic syndrome
Loop diuretics to offset sodium retention (careful to avoid hemoconcentration because patients are at risk for thromboembolic events)
How does hypoalbuminemia affect nephrotic syndrome?
hypoalbuminemia decreases available binding sites for drugs and increases circulating levels of unbound drugs
NEPHROLITHIASIS Assessment: • stones in the renal pelvis are
are painless unless complicated by infection or obstruction
NEPHROLITHIASIS what happens
a stone passage through the ureters produces flank pain radiating to the groin with nausea and vomiting •
NEPHROLITHIASIS: What can be seen with passage
hematuria can be seen with ureteral passage
NEPHROLITHIASIS: Treatment
Treat underlying disorder • maintain daily uop > 2-3l/day
TURP Hypervolemia can result from ________ leading to HBP
absorption of irrigants→
htn, bradycardia, pulmonary edema
TURP hyponatremia can result from _______ leading to
CAP-CS
absorption of na free irrigants→
Confusion, Agitation, pulmonary edema,
CV collapse, Seizures
2 issues that may occur with TURP
Hypervolemia
Hyponatremia
TURP Ace inhibitors →
increased risk of intraoperative hypotension
ANESTHESIA AND RENAL DISEASE
Volatile anesthetics →
decreased RBF GFR, and UOP by causing a drop in
BP and CO (transient)
ARF official diagnosis Criteria
FORMAL DIAGNOSIS:
• INCREASED SERUM CREATININE MORE THAN 0.5 MG/DL OF BASELINE
• 50% DECREASE IN CREATININE CLEARANCE
• A CHANGE IN SERUM CREATININE OF GREATER THAN 0.3 MG/DL WITHIN 48 HOURS OF
ACUTE INSULT
ANESTHESIA AND RENAL DISEASE: Painful stimuli
Painful stimuli → increased ADH secretion
ANESTHESIA AND RENAL DISEASE- How PPV impact
Positive pressure ventilation→ decreased ANP secretion → oliguria
Renal transplantation: Kidney from a cadaver
a kidney from a cadaver can be preserved by perfusion at low temperatures for up to 48 hours •
Renal Transplantation what must be matched?
HLA antigens and ABO blood groups must be matched •
Renal transplantation , donor kidney ?
donor kidney is placed in the lower abdomen and receives its vascular supply from the iliac vessels •
Renal Transplantation , when is immunosuppresion therapy started?
immunosuppression therapy is started perioperatively
Long-term immunosuppression results in _____And frequency of _______
opportunistic infections
frequency of cancer is 30 to 100 times higher
Treatment of acute immunologic rejection
Removal of the transplanted kidney, especially if accompanied by DIC
What are the delayed signs of graft rejection (FLD)
Fever
Local tenderness
Decreased UOP
Meds and therapy for Treatment of acute immunologic rejection (CAH)
Corticosteroids
Antilymphocyte globulin
Hemodialysis
ESRD and its effect on oxygen dissociation
CRF Signs and symptoms 1. Electrolyte imbalances:
hyperkalemia, hypermagnesemia, hyperphosphatemia, hypocalcemia
ESRD and its effect on oxygen dissociation
CRF Signs and symptoms 2. Metabolic acidosis. Anemia
a. Anemia • increased co, right shift of oxyhemoglobin dissociation curve
ESRD and its effect on oxygen dissociation Bartter syndrome = What is it?
Ccongenital hypokalemic alkalosis)- autosomal recessive
How oxygen dissociation is affected with Bartter syndrome? KPL-VI
- k+ follows H+
- pH and O2 dissociation curve→ less O2 available to tissues
- volume depletion from Na+ wasting
- increased Prostaglandins → activate renin/angiotensin/aldosterone axis (RAAS)
Bartter Syndrome move the O2 dissociation curve to the
LEFT
Sevoflurane is metabolized to
Fluorine (F-)
Sevoflurane leads to
transient tubular dysfunction (concentrating ability, increased β-n-acetylglucosaminidase) •
Effect of renal disease on anesthesia drugs Sevoflurane, is there changes in BUN or Cr? What about compound A?
no change in cr- or bun • Compound A- questionable significance •
Effect of renal disease on anesthesia drugs: ACE
Increased risk of intraoperative hypotension
Effect of renal disease on anesthesia drugs disrupted bbb and less protein binding →
increased bioavailability of induction drugs
Effect of renal disease on anesthesia drugs “ gastric
Delayed Gastric emptying
K release after succ is how much ? Does defasciculation change K+ release?
• k+ release after sux (0.5 to 1.0 meq/l) de-fasiculation does not change k+ release
CHRONIC RENAL FAILURE • Perioperative anesthesia considerations AVOID ➔
NSAIDS
Why do we avoid NSAIDS with CRF? HPI
Exacerbate →
HYPERTENSION
PRECIPITATE EDEMA, AND
INCREASE THE RISK OF CV COMPLICATIONS WITH ESRD.
Chronic renal Failure and Opioids
USE PARENTERAL OPIOIDS JUDICIOUSLY.
Acute Renal FAILURE: Give at lower dose based on GFR: CoFeKeMMM
CODEINE FENTANYL KETOROLAC, MEPERIDINE METHADONE MORPHINE.
Acute Renal FAILURE Do not require dosage adjustments→ ARS
Alfentanil
Remifentanyl
Sufentanyl
Acute Renal FAILURE avoid further renal insults
hypovolemia, hypoxia, nephrotoxins
ARF Perioperative anesthesia considerations dialysis
within 24 hours of elective surgery.
CHRONIC RENAL FAILURE
• PERIOPERATIVE ANESTHESIA CONSIDERATIONS
13 Drugs that rely heavily on renal elimination: (VENGA- HAMCCPSV)
VECURONIUM EDROPHONIUM NEOSTIGMINE, GLYCOPYRROLATE, ATROPINE, HYDRALAZINE, AMINOGLYCOSIDES MILRINONE, CEPHALOSPORINS, CODEINE PENICILLINS SULFONAMIDES VANCOMYCIN,
Chronic Renal Failure Drugs that have active metabolite and its implications.? MMH
Meperidine, Morphine, and Hydromorphone with active metabolites ➔ accumulate in ESRD
Chronic Renal Failure Best paralytics ? What may be delayed?
Atracurium and cisatracurium (best choice paralytics), but LAUDANOSINE clearance maybe delayed.
CRF and serum potassium
serum potassium should not exceed 5.5 meq/L
LR and CRF
LR has 4 meq/L of potassium
Reno-protective pharmacological agents Perioperative anesthesia considerations→low dose fenoldopam
➔ renal vasodilation
Reno-protective pharmacological agents
Perioperative anesthesia considerations mannitol ➔
renal prostaglandins produced ➔ renal vasodilation
Reno-protective pharmacological agents Perioperative anesthesia considerations N-acetylcysteine ➔
free radical scavenger ➔ protect against radiographic dye-induced nephropathy
Hemodialysis: mainstay of treatment d/t .
volume overload, hyperkalemia, severe metabolic acidosis, symptomatic uremia, and overdose with a dialyzable drug
Reno-protective pharmacological agents best choice and why?
Selectively constrict renal efferent arterioles ➔ preserve gfr and uop_
Reno-protective pharmacological agents best choice and why?
Selectively constrict renal efferent arterioles ➔ preserve GFR and UOP
2 main things that mannitol doses
Scavenges Free radicals
Release prostaglandins, causing vasodilation
Herbal Supplements that Decrease Platelet Aggregation
BB D FFF GGGGS
- Bilberry
- Bromelain
- Dong Quoi
- Feverfew
- Fish oil
- Flax seed oil
- Garlic
- Ginger
- Gingko biloba
- Grape seed extract
- Saw palmetto
Herbal Supplements that Inhibit Clotting
DDHCC
- Dandelion root
- Dong Quoi
- Chamomile
- Curcumin
- Horse chestnut
Hemodynamic effects of prone position
Do not administer excessive
crystalloid volume to promote urine output.
Hemodynamic effects of prone position Urine output is
often less than expected when patients are positioned prone
Prone CPR and SBP
Increase in systolic BP
Prone CPR and circulation
good circulatory and respiratory support, easy to perform
Prone and GFR
Increased intra-abdominal pressure may decrease GFR.
Prone , Pressure transmitted to
epidural veins, increased bleeding.
Prone : In the absence of cord compression,
modest decrease in BP may be helpful, when extensive surgery is anticipated
This can be accomplished with anesthetics and opioids or by the use of beta blockers and SNP
BP approximately
20% below patient lowest recorded BP when awake
PRONE: MAP
> 60 mm Hg in youg patients and
MAP> 80 mm Hg in elderly pts
Prone and ↓ BP may be due to
abdominal compression and decreased venous return
Prone and ↑ Blood loss
2º to epidural vein engorgement abdominal compression or vascular injury
Acute ↓ BP may be due to a
vascular injury either obvious or occult until proven otherwise.
Prone: If ↓ BP persists despite vigorous blood and fluid administration, what would you suspect?
RETROPERITONEAL BLEEDING
Risk Factors for POVL (MOHP)
Male
Obese
Hypertension and Peripheral Vascular disease
Prolonged procedures, Substantial bloodloss or Both
Recommendations to prevent POVL
Blood pressure management
• Assess the patient’s baseline blood pressure.
• Continually monitor systemic blood pressure in high risk patients.
Treat prolonged significant decreases in blood pressure.
Recommendations to prevent POVL : Determine
and discuss
• Determine on a case-by case basis whether deliberate hypotension should be used in high-risk patients.▪ Discuss with the surgeon whether deliberate hypotension is necessary.
Recommendations to prevent POVL Management of Blood Loss and Administration of Fluids Periodically monitor
hemoglobin or hematocrit values during surgery in high-risk patients who experience substantial blood loss.
Recommendations to prevent POVL : Continual monitoring of
▪ Continual monitoring of hydration levels to avoid overhydration
▪ Fluid replacement limitation.
Recommendations to prevent POVL
Use of Vasopressors
Adrenergic agonists may be used on a case-by-case basis when it is necessary to correct for hypotension
Recommendations to prevent POVL Patient and Head Positioning Devices
Positioning the patient so that the head is level with
or higher than the heart
Recommendations to prevent POVL eyes
Avoidance of direct pressure on the globe of
the eye
Recommendations to prevent POVL Maintaining of face in a
neutral forward position(e.g., without significant neck flexion or extension, lateral flexion, or rotation)
Recommendations to prevent POVL Staging of Surgical Procedures
Use of staged procedures for spine surgery when
anticipated length is greater than 6 h
Rheumatoid arthritis: What is it?
it is a autoimmune condition, immune mediated joint destruction with chronic and progressive inflammation of synovial membranes
RA patients implications
these are the really involved and difficult patients,
affects multiple organ systems
RA and Cardiovascular – PMCCVA
Pericardial thickening and effusion Myocarditis Coronary arteritis Conduction deficits, Vasculitis and cardiac valve fibrosis Aortic regurgitation)
RA and stress test Arthritis
limits exercise probably cant get treadmill ECHO, so dobutamine ECHO may be needed
RA → HTN / cardiovascular disease and c
Conduction defects common in elderly leads to dysrhythmias leads to falls then Hip fracture
If patient has RA, at a minimum get
get EKG at minimum , if tamponade or severe CV disease suspected - ECHO
RA and respiratory what is common, and what is rare, and if rare presents, what are the symptoms (CDS) Get these tests___
Pulmonary effusions common, rare to have Pulmonary fibrosis, if present will have cough, dyspnea, SOB-
PFTs,
RA and airway derangements
Cricoarytenoid joints
Glottic narrowing
Arthritis and TMJ
Arthritis of TMJ – limited mouth opening
Arthritis of TMJ implications? What is needed.?
making direct laryngoscopy difficult and may need fiberoptic if intubating
RA have cricoarytenoid joings, glottic narrowing, anesthesia considerations?
– Use smaller ETT – presenting sign hoarseness, worry about post extubation stridor even with smaller ETT
Neurological and RA
Check for Full ROM –
nerve root compression and cerebral ischemia from vertebral artery compression
RA : Position and Musculoskeletal
Pain and arthritis make positioning and regional uncomfortable and more difficult
RA and small joints and implications
Affect small joints causing deformity like in hand, wrist and feet - Difficult to place arterial line or IV
Hematologic and RA
Anemia from NSAID gastritis and renal toxicity
Eosinophilia
RA HGB if less than 12
HGB if less than 12 consider autologous blood donation as Hip fracture has the potential for large volume loss +1 L
RA has PLT dysfunction why?
from aspirin therapy and thrombocytopenia
RA and Endocrine
adrenal insufficiency ( from glucocorticoid therapy and impaired immune system
RA and Dermatological
Thin and atrophic skin from the disease and immunosuppressive drugs so just make sure pressure points are padded well so don’t get skin breakdown
RA –If pt has severe RA: Means patient is on
steroids, immune therapy or methotrexate
RA patient get xrays ? which type and why?
Especially lateral views of neck
Atlantoaxial subluxation instability, which is diagnosed by an x-ray, can compromise vertebral blood flow and compress spinal cord and brainstem,
RA patients with Xray showing Atlantoaxial subluxation instability, What do you do?
Intubate one of these patients - do so using fiberoptic laryngoscope.
PTS W/RHEUMATOID ARTHRITIS MAYBE ON
ORAL CORTICOSTEROIDS AND SUPPLEMENTAL PERIOPERATIVE STEROIDS
RA and Adrenal insufficiency
Adrenal insufficiency from steroids therapy, supplemental intraoperative steroids
AC and Regional Warfarin
Hold for 4-5 days prior to block
Removed catheter with INR < 1.5, INR >3 hold dose
AC and Regional→ ASA
NO CONTRAINDICATIONS
AC and Regional→Clopidogrel
stop 7 days prior, if neuraxial considered between 5-7 days,restoration of platelet function should be confirmed.
AC and Regional→ Prasugrel ,
stop 7-10 days, wait 9 hours after neuraxial block or catheter removal before administration of drugs
AC and Regional → Ticagrelor
stop 5-7 days prior to neuraxial ,wait 10 hours after neuraxial block or catheter remove before administration of drug
AC and Regional→ Ticlopidine
Stop 14 days prior to neuraxial block
AC and Regional→ LMWH : Preop
wait 10-12 hours after prophylactic dose, 24 hours after tx dose
AC and Regional→ LMWH Post op
catheters removed at least 2 hours prior to initiation of dose of 2x daily
AC and Regional→ For single daily dose of LMWH ,
catheters can be maintained but should only be removed 10-12 hours after last dose
AC and Regional →Heparin SC < 10000 units per day
NO contraindications
AC and Regional→ Heparin SC >10000 Units per day
use caution- Check platelet if on heparin > 4 days
AC and Regional→ Dabigatran
stop 5 days prior to neuraxial block, wait 6 hours after neuraxial block or catheter removal before adminis ofdrugs
AC and Regional→ Apixaban,
Stop 3 days prior to neuraxial block, wait 7 hours after neuraxial block or catheter removal
AC and Regional→ Rivaroxaban
stop 3 days prior to neuraxial block, wait 8 hours after neuraxial block or catheter removal
AC and Regional Thrombolytics/Fibrinolytics, thrombin inhibitors:
CONTRAINDICATED
Regional contraindicated
TPA contraindicated
Bone Cement Implantation syndrome. Methymethacrylate (MMA): Cause is not completely known. Some speculate it
from micro emboli forming during cementing, others believe its from histamine release, complement activation, and vasodilation.
In BCIS, Intense
exothermic reaction causes heat and results in intramedullary hypertension which can cause fat, bone marrow, cement and air embolization into venous circulation.
MMA is not usually used in
younger patients and those physically active, just press fit which means just forcibly seated with mallet into femur opening.
BCIS Etiology
not completely understood
BCIS Most common with
hip arthroplasty, but also can occur with knee cementing and vertebroplasty.
BCIS Occurs in
2-17% of cementing surgeries
BCIS Risk factors – PPAD
preexisting CV disease
preexisting Pulm. HTN,
ASA 3 or greater,
depends on type of fracture and surgical technique
S/S of BCIS : HIHAP-D
Hypoxia Increased pulmonary shunt) Hypotension Arrhythmias (including heart block and sinus arrest), Pulmonary hypertension (increased pulmonary vascular resistance) Decreased cardiac output.
BCIS Treatment: Cementing time
should be recorded in chart and communication at cementing time is crucial as prior to cementing,
BCIS Treatment BP needs to be
optimized, FiO2 100% and pressure bags for fluids if needed.
BCIS Treatment If hypotension occurs use
Alpha agonist – phenylephrine for hypotension and aggressive fluid resuscitation
DVT Venous Thromboembolism /PET
Without prophylaxis – DVT in
40-80% of orthopedic pts.
Multimodal prophylaxis protocol for THA in one study had DVT and PE rates of
2.5% and 0.6% which much lower than the numbers above.
DVT Risk factors include OPAULI
Obesity Procedures lasting more than 30 min Age greater than 60 years Use of a tourniquet Lower extremity fracture Immobilization for more than 4 days.
Patients at greatest risk for DVT include those undergoing
hip surgery and knee replacement or major operations for lower extremity trauma
DVT and Preventative:
America College of Chest Physicians guideline recommend a minimum 14 days of pharmacologic thromboprophylaxis and / or SCD device to decrease risk
DVT and regional anesthesia
The use of neuraxial anesthesia, which causes vasodilation in the lower extremities, reduces the incidence of DVT by 50% in comparison to general anesthesia.
Complications: BLEEDING: Deliberate Hypotension
Deliberate hypotension using neuraxial anesthesia during hip surgery decreases blood loss and intraoperative transfusion needs when compared to general anesthesia
Tranexamic acid (TXA) can be
given intravenously or topically in the perioperative setting to decrease blood loss and transfusion requirements
What can improve intraoperative coagulation?
Maintaining normothermia improves intraoperative coagulation
Orthopedic syndrome Fat embolism syndrome classically presents
within 72 h following long-bone or pelvic fracture,
TRIAD of PE (PCD)
Petechiae
Confusion
Dyspnea
Fat embolism Petechia location (ACU)
Axilla, Chest, UE
FAT embolism signs w/ GETA –P
decline in ETCO2
decline arterial oxygen saturation and rise in PA
FAT embolism mortality
10-20% mortality
FAT embolism Treatment: SOPR
Stabilization and surgery on fracture,
Oxygen therapy especially CPAP to prevent hypoxia, Pressors in hypotension and vasodilators may help
Pulmonary HTN
Respiratory support
FAT embolism useless and controversial
steroids are controversial and heparin is not effective
What is Venous Air embolism ?
Potential hazard whenever the operative site is above the level of the heart such as a shoulder surgery in beach chair position, or hip replacement when pt. is on their side.
VAE: Most sensitive monitor
TEE
VAE of S/S: (SIRI)
Sudden decrease in ETCO2
Increase in PAP, RV
Decrease in CO and BP
Increased dead space
Treatment of VAE (IFLAT) TAGS
Inform surgeon
Flood area with saline
Lower preoperative sites
Apply occlusive dressing to all bone edges if possible Try to identify air entry, if possible
Try aspiration thru right atrial catheter
Avoid PEEP
Give O2
Stop nitrous if on
VAE treatment Support hemodynamics with
Pressors and fluids
Lateral position and air exchange
Pulmonary shunting involved in lateral position
Positioning and how it affects MAP in different organs
Decreased CI, CVP, PCWP, and increased SVR
MAP and SITTING UP
Increases SVR
Postural DECREASE IN BP
45 degree head up and hemodynamics
(minimal hemodynamic changes)
90 degree head up and hemodynamics
CO decrease by 20% due to venous pooling of blood in legs
Excessive flexion of neck can
impede arterial and venous blood flow and cause hypoperfusion and inadequate drainage of the brain
Kinked tube due to neck flexion,
risk of tube pressure on tongue leading to macroglossia. Keep two fingerbreadths between chin and sternum
The sitting position interferes
the least with ventilation and has less influence on lung volumes
With flexion of the hips and elevation of the legs
abdominal contents may shift caudally and limit the diaphragm, which will decrease FRC
Arm support to prevent stretching
of brachial plexus
Leg support/flexion of knees to prevent
stretching of sciatic nerve
Venous pooling in lower extremities
VPQP
Venous Air Embolism (VAE),
Pneumocephalus
Quadriplegia
Peripheral nerve injuries
Conversion factor: 1 cm rise =
0.75 mmHg drop in MAP
MAP 5020 cm rise = 15mmHg DROP in MAP = 65mmHG
Patients in the deck chair position are prone to .
hypotension, mainly due to venous pooling in the extremities and lack of surgical stimulation with an effective block.
The angle of elevation from the waist should be
increased slowly in the compromised patient, thus allowing time for haemodynamic equilibration
Intra-operative cerebral ischemia has been reported, probably through changes in
cerebral blood flow from a combination of postural hypotension and excessive head and neck manipulation
MAP increases or decreases by
0.75mmHg for each cm change in height between heart and a body region.
MAP increases or decreases by 0.75mmHg for each cm change in height between heart and a body region. Therefore region
elevated above the heart in the sitting, head-up or lithotomy position may be at risk for hypoperfusion and ischemia, especially with hypotension.
Try to elevate torso in increments
giving the body time to adjust.
Often used to support head using straps or tape to secure head to the headrest - note risk of brachial plexus injury with manipulation of limbs/head
Horse shoe head rest
TURP and Spinal
Spinal is considered the anesthetic of choice
Why is spinal better for TURP?
Early signs and symptoms of TURP syndrome, hypervolemia, and bladder perforation can be easily detected in a responsive patient.
Other benefits of SPINAL In TURP (LDE)
Less blood loss
Decreased incidence of postoperative venous thrombus
Embolus
Spinal anesthesia level for TURP
T10 sensory level is a must for adequate anesthesia
Incidence of PDPH
very low in this age group
Spinal for TURP Medication:
0.75% bupivacaine, 12 mg in 7.5% dextrose solution (1.6 mL)
The nerve supply to the prostate originates from the
inferior hypogastric plexus and carries both sympathetic fibers from T11 to L2 and parasympathetic fibers from S2 to S4.
Pain signal from bladder distension travels along with
T11 to L2 sympathetic fibers.
Considering this innervation, height of regional block up to
T10 is sufficient for TURP
Jaffe recommends T9 level, but Higher level of block may
mask the pain if perforation of the prostatic capsule should occur.
TURP Spinal meds commonly included with LA.
Intrathecal opioids (fentanyl or sufentanil)
TURP and Continuous lumbar epidural anesthesia
has no advantage during TURP-procedure relatively short and supplemental dose usually not necessary
TURP and Fluids
Cautious fluid loading may be used to minimize spinal anesthesia-induced hypotension, but if patients cant tolerate this or need pulmonary support perform GA
TURP Advantage of Regional anesthesia- In the awake patient-classic Triad of symptoms- TURP syndrome
increase in both systolic and diastolic pressures (increase in PP), bradycardia, and mental status changes.
Advantage of Regional for TURP
GAPU
Good post op analgesia
Allows to monitor level of consciousness and detect early signs of TURP syndrome
Possible reduced blood loss
Useful in patient with significant respiratory disease
Regional advantage with perforation
Earlier recognition of bladder perforation or CAPSULAR TEAR
Disadvantage of Regional
Does not prevent penile erection which can interfere with surgery.
High Prevalence of BPH is in which zone
transitional ZONE
MOST BLOOD
Dorsal VENOUS COMPLEX-
Anesthetic approach to TURP
Respiratory
COPD common-if patient has a > 50 pack-year history, or any respiratory symptoms-consider PFTs, ABG, or CXR
Anesthetic approach to TURPCardiovascular
CAD, CHF-exercise tolerance needs to be assessed-
TURP and Cardiac patient should be able to
Climb a flight of stairs without difficulty or SOB, EKG, check history of pacemaker.
TURP Neurologic
CVD or Alzheimer’s common-assess baseline mental status to guide evaluation of any intraop or postop changes.
TURP and Renal
Renal impairment should be anticipated secondary to chronic obstruction. Check BUN, Cr, Cr clearance, and electrolyte values.
Hematologic and TURP
Moderate blood loss should be expected with l
Larger glands and T and C is indicated.
TURP, when is Type and cross NOT NECESSARY
If gland < 80 g, not necessary. Check CBC/coags
TURP premedication CV : Continue those medications DiNB and which medication for anxiety
Continue commonly used drugs (digitalis, BB, NTG) to prevent CV problems.
Midazolam 1-2 mg IV prn for anxiety.
TURP preop evaluation goal
Surgical population generally elderly may have preexisting medical problems-preop evaluation should be directed toward detection and treatment of these conditions.
TURP and Pacemaker-must be
converted to a fixed rate unless they are designed to operate in presence of applied currents.
TURP Induction:
Can use LMA, but lithotomy position with head down tilt decreases FRC and has increased risk for aspiration.
TURP and Maintenance-muscle relaxation a
not mandatory,
TURP, what must be avoided and why?
patient movement during procedure must be avoided-can lead to perforation or injury to the external sphincter-postop incontinence.
TURP and The obturator
The obturator nerve passes in close proximity to the inferolateral bladder wall, bladder neck and lateral prostatic urethra.
During TUPR resection in these areas may result in
stimulation of the obturator nerve, causing adductor contraction (obturator reflex) and possible inadvertent bladder perforation.
Shortcoming with subarachnoid block with TURP is
sparing of this nerve (Obturator nerve)
To successfully prevent this injury to Obturator nerve
Ultrasound guided obturator nerve block or injecting a local anesthetic into the sensitive area through a special needle passed through the resectoscope
TURP If using GA consider
succinylcholine or rocuronium-can be rapidly reversed using Sugammadex (4-8mg/kg).
With TURP Want to give minimal amounts of IV fluids why?
Minimize fluid overload due to possible irrigation absorption.
TURP Anticipate decrease BP
when legs are repositioned from lithotomy position.
TURP Avoid stress on lumbar spine by
Slowly and simultaneously bringing legs together and returning to supine position
With TURP Solutions should
not be hung higher than 30 cm above the operating table at the beginning of the procedure and higher than 15 cm during the final stages-decreases fluid absorption.
TURP Should
not exceed 2 hrs-Uptake of 1 L of irrigant into the circulation within 1 hour can decrease the serum sodium 5-8 mEq/L-limiting resection time to 1 hours is ideal.
TURP, May want to avoid this position and why ?
Tredenlenburg; promotes fluid absorption
Questions to consider with TURP
- What is the irrigation fluid?
- What is the bag height over the prostate?
- What is the size of the prostate?
- What is the expected duration of procedure?
- What is the surgical operating position?
Systemic absorption of the irrigation fluid directly through
the prostatic venous plexus, or more slowly through the retroperitoneal and perivesical spaces.
TURP and fluid reabsorption Average of
10-30 mL of fluid can be absorbed per minute of resection time, and 6-8 L can be absorbed in cases that last up to 2 hours.
TURP Complications of absorption: HDVCRT
Hypoosmolality
Dilutional hyponatremia
Volume overload with pulmonary edema,
Cardiac effects
Retinal toxic effects (with glycine), and
Transient hyperglycemia/hypokalemia with glucose
irrigation solutions.
TURP signs and Symtpoms
General Anesthesia-CNS symptoms
are hidden under general anesthesia.
TURP SYNDROME Can see (ABC-VA)
Arrhythmias Bradycardia Cyanosis, Vagal response And unexplained hypotension or hypertension
TURP Intravascular Volume Expansion
Systemic HTN and reflex bradycardia-pulmonary edema
TURP and Intravascular Volume Loss
H20 flux along osmotic and hydrostatic pressure gradients out of the intravascular space and into lungs-pulmonary edema and hypovolemic shock
TURP and Dilutional Hyponatremia
Osmotic shift of fluid->cerebral edema, increase in ICP, and CNS symptoms.
TURP and Hypoosmolality
BBB freely permeable to water->cerebral edema, increased ICP->bradycardia and HTN
TURP Hyperammonemia
Oxidative deamination of glycine to glyoxylic acid and ammonia
TURP and Hyperglycinemia
Deterioration of vision-transient blindness.
Robotic surgery Positioning
Different positioning
increases risk for nerve injury
Improved nerve sparing
Robotic surgery Positioning
Different positioning Taped or strapped to bed frame to
prevent movement in steep Trendelenburg, increased risk for pressure points/nerve damage
Robotic surgery Positioning Trocars ? what is crucial
are fixed and can cause injury if patient moves-NMB crucial
Increased risk of aspiration
Robotic surgery Trendenlenburg Respiratory stress –
patients with significant hx of lung disease cannot tolerate
Robotic surgery Trendelenburg position -
CO decreased by 10-30%, pts with preexisting HD can lead to ischemia/dysrhythmias
Robotic surgery Pneumoperitoneum can cause
extreme brady or asystole
Robotic surgery Trendelenburg RBF and GFR
decreased/ADH and aldosterone increased
Lithotomy with stirrups/boots (Less extreme than Trendelenburg)
CC300
Compartmentsyndrome/thrombus/Sciatic/obturator/femoral/peroneal/saphenous
Cephalad movement of diaphragm/ck ETT
300 ml auto return
Steep Trendelenburg
(more extreme changes from Lithotomy)
Lithotomy with stirrups/boots
(Less extreme than Trendelenburg)
Steep Trendelenburg advantage
Optimizes organ visualization
Steep Trendelenburg Hemodynamic changes CARDIAC (LSV)
Left ventricular filling pressure and CO decrease
Systemic vascular resistance and MAP increase
VQ mismatch
Steep Trendelenburg Hemodynamic changes RESPIRATORY D-CLF LVUPR
Decreased compliance
Decreased lung volume
Decreased FRC
Limited diaphragm movement VQ mismatch upper airway edema pulmonary edema Regurgitation – place OGT
Steep Trendelenburg CNS
Increased intracranial/Brain edema and intraocular pressure
Steep Trendelenburg- 3 extra interventions with arms (BBP)
Bilateral arms tucked at sides
Beware of fingers/table down
Padded arms/ulnar nerve/eyes (also taped)
Steep Trendelenburg/Pneumoperitoneum/Respiratory compromise Intervention: (PDI)
Pressure control
Decreased tidal volume,
Increased RR to maintain ETCO2
After intervention,
watch for decrease in insufflation or
change from Trendelenburg to flat -> decrease pressure!
Facial and airway swelling (Steep Tren) -
confirm airway movement BEFORE extubating
What happens with Spondylothesis
Anterior Subluxation
Epidermolysis BULLOSA which anesthesia preferred
Regional Anesthesia
Myotonic Dystrophy
General anesthesia doesn’t stop contraction
Clinical Features of Familial Periodic Paralysis : Factor with Both HYPOKALEMIA and HYPERKALEMIA
Hypothermia
Good response to anticholinesterase (MG vs MS)
MG
Sensitive to both succ and NDNMB (MG vs MS)
Myasthenia Syndrome
How does kyphoscoliosis affect ?
Anterior + Lateral flexed spinal column
Manifestations of Myasthenic Syndrome ProLA ES MC RAD
Proximal limb weakness (Legs more than arms)
Exercise Improves stength
Muscle pain common
Reflexes absent or decreased
Manifestations of Myasthenia Gravis FOB EF MU RN
Extraocular,bulbar and facial muscle weakness
Exercise causes fatigue
Muscle pain uncommon
Reflexes normal
Myasthenic syndrome Gender more affected M/F
Affect males more often than females
Myasthenia Gravis more affected M/F
Affect females more often than males
Myasthenic syndrome Co-Existing Pathologic conditions
Small cell lung cancer
Myasthenia Gravis Co-Existing Pathologic conditions
Thymoma
Myasthenic Syndrome RESPONSE to muscle relaxants
Sensitive to succ and NDNMB
Myasthenic Syndrome RESPONSE to Anticholinesterases
POOR
Myasthenia GRAVIS RESPONSE to muscle relaxants
Resistant to Succ, Sensitive to NDNMB
Myasthenia GRAVIS RESPONSE to Anticholinesterases
GOOD
H2 Blockers
Cimetidine, famotidine, -tidine
ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS and ANGIOTENSIN RECEPTOR
BLOCKERS (ARB) ➔
MPROVE INTRARENAL HEMODYNAMICS and HAVE RENOPROTECTIVE QUALITIES.
During a renal transplant which vessel supply the new graft?
Iliac artery
Where in the nephron is most of the blood reabsorbed?
PCT
What is spondylolisthesis?
Anterior subluxation of vertebrae
A patient with CREST syndrome is at risk for what during anesthesia?
Aspiration
What is a clinical feature of Myasthenia Gravis
Bulbar muscle weakness
CURCUMIN effects
Increase (Prolonged) aPTT, PT significantly Inhibit thrombin (II) and Factor Xa
Complications of Prone position with Airway
ETT kinking, dislodgment
Upper airway edema.
Complications of Prone position with NECK
Hyperextension or hyperflexion.
-Cervical rotation: compromised blood flow to brain
Complications of Prone position with EYES
-Orbital pressure->central retinal artery occlusion,
supraorbital nerve.
-Corneal abrasion
Complications of Prone position with ABDOMEN
Pressure transmitted to epidural veins, increased bleeding.
Complications of Prone position with UE
Brachial plexus stretch. -Ulnar nerve compression.
Complications of Prone Position with LE
Flexion of hips: occlusion of femoral vein, DVT, kinking of vascular grafts
–Pressure lateral to fibula: peroneal nerve palsy
Pressure on iliac crest—lateral femoral cutaneous nerve.
In Prone position , Flexion of hips lead to (KOD)
Kinking of Vascular grafts
Occlusion of femoral vein
DVT
In Prone position, Pressure lateral to fibula leads to
peroneal nerve palsy
In Prone Position, Pressure on Illiac Crest leads to
Lateral femoral cutaneous nerve damage
TURP Important to determine
Size of the enlarged prostate or adenoma must be carefully assessed before the surgery, usually with cystoscopy, to determine if the procedure can be completed within two hours (ideally 1 hr or less). If unable, open prostatectomy should be performed to prevent TURP syndrome
ROBOTIC SURGERY ADVANTAGE BIS Improved nerve sparing Blood loss Hospital time \_\_\_\_\_\_continence Improved \_\_\_\_\_\_\_\_rate Incisions? Scaring post op pain? infection? omplications?
Improved nerve sparing < Blood loss < Hospital time Enhanced continence Improved impotency rate Small incisions/Less Scarring Less post op pain Decreased infection Fewer complications
Ascending permeable to _____and not to _______
NaCL not to H2O
Region permeable to Water?
PCT and descending
Water and% absorption in each section
PCT 60-70% and NaCL
Loop 25% and NaCL
DCT 5% influenced by ADH
Collecting Variable influenced by ADH
3 most common complications of Prone
Post Operative vision loss
Cardiovascular compromise
Venous Air Embolism
Myasthenic Syndrome suspected for lung cancer patients undergoing, bronchoscopy, thoracoscopy and mediastinoscopy and WHAT ELSE SHOULD BE CONSIDERED> ?
Need to decrease doses of muscle relaxants should be
T10 for TURP why
T10 level, because the stretch receptors in the distended bladder cause pain higher than the coverage needed for bladder surgery.
Na replacement for TURP syndrome
100ml/hr of 3% hypertonic saline
D/C when Na>120
