Monthly Archives: February 2017

INTRACRANIAL PRESSURE ( #ICP ) MEASUREMENT & HOW IT CAN GUIDE THERAPY❓

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🔸ICP data can be used to

✔️predict outcome and evolution of intracranial pathology
✔️calculate and manage cerebral perfusion pressure (CPP) [without an ICP monitor, CPP is not known].
✔️direct management strategies, and
✔️limit the use of potentially deleterious therapies.
🔸Cerebral herniation is a pressure issue and an ICP monitor may allow early detection; it is preferable to avoid herniation than to treat it
🔸Information from an ICP monitor may provide useful information to guide patient care. For example, a patient with a worrisome-appearing CT scan who does not have intracranial hypertension may not require the same degree of treatment as a patient with a similar scan but elevated ICP. Similarly, a patient with elevated ICP that is refractory to escalating management becomes an early candidate for “second tier” treatments or if very high, even withdrawal of care.
🔸ICP values have prognostic value and so it can guide management and discussions with the family about outcomes
🔸Even transient episodes of severely raised ICP and ischemia can be devastating to the traumatized brain, making it critical to accurately and continuously monitor ICP & CPP. Because insertion of intraparenchymal ICP monitors is safe, the ability to monitor CPP per se is a supportable argument for widespread ICP monitoring.
🔸Perhaps more important than a single ICP threshold may be a trend over time, ICP waveform analysis, or whether the ICP value is associated with other detrimental effects.
🔸When both ICP and brain oxygen are treated, the outcome may be better than if just ICP is treated after TBI
🔸The ICP waveform is a modified arterial pressure tracing
🔸 It has 3 peaks: P1, P2 & P3
🔸 P1 is a result of transmitted pressure from choroid plexus
🔸 The amplitude of P2 changes with brain compliance. If compliance is poor, amplitude will be high ( can even exceed that of P1) and vice versa
🔸P3 represents the dicrotic notch
🔸 Lundberg (A) or Plateau waves are steep rise of ICP to over 50 mm of Hg and lasting for 5-20 minutes; then it falls abruptly. Are Always pathological and indicates significantly reduced compliance
🔸 Lundberg (B) waves are oscillations occurring every 1-2 minutes where ICP rises to over 20-30 mm of Hg from baseline in a crescendo manner. They are supposed to be result of altered cerebral (B)lood volume and altered tone of cerebral (B)lood vessels
🔸 Lundberg (C) waves are oscillations whose amplitude is less than that of B waves and are supposed to result because of interactions between cardiac and respiratory (C)ycles. They occur also in healthy individuals
METHODS OF MEASUREMENT OF ICP
➿ Intraventricular catheter – ventriculostomy represents the “gold standard” for pressure measurement

✔️Normally placed in the frontal horn of lateral ventricle
✔️Allows therapeutic CSF drainage
✔️Creates a pathway for infection
✔️In case of the Integra Neuroscience external drainage catheter, ICP readings are based on a fluid-filled transduction system that transmits changes in ICP through a saline-filled tube to a diaphragm on a strain gauge transducer. This monitor must be leveled with the foramen of Monro (approximately the level of the external auditory canal) after insertion and should be zero-balanced daily. The level of the drain can be adjusted to allow more or less CSF drainage.
➿Subdural bolt / Catheters
✔️ less invasive
✔️ Bolts commonly use fiberoptic technology that allows continuous ICP monitoring without CSF drainage. The fiberoptic type of catheter can be placed in the subdural space or in the brain parenchyma
✔️ Usually subdural space over frontal lobe of non-dominant hemisphere is selected
✔️ Prone to signal damping and calibration drift
✔️ Potential risk of infection
✔️ Doesn’t require penetration of brain tissue
✔️Camino Post Craniotomy Subdural Pressure Monitor utilizes the craniotomy bur holes and flap as a point of entry. The monitor is zero-balanced and then tunneled under the scalp toward the craniotomy bur hole of choice and positioned in the subdural space. This monitor contains a microtransducer at the tip, which is similar to the OLM ICP monitor ( see below)
✔️Gaeltec ICT/B pressure sensor is intended to monitor ICP subdurally. It contains a balloon-covered pressure sensor that is activated when filled with air. This monitor is self–zero-balanced in vivo and is reusable.
➿Intracerebral transducer
✔️Parenchymal devices are easier to place, particularly when altered ventricular anatomy may limit ventricular catheter placement.
✔️However, intraparenchymal fiber-optic and electronic strain gauge systems are more expensive and cannot be recalibrated once in situ
✔️Inability to check zero calibration & drain CSF
✔️ Risk of infection
✔️Less reliable
✔️The Camino OLM ICP monitor measures ICP in the intraparenchymal tissue or subarachnoid space. It contains a transducer at the distal tip, thus measuring pressure without a fluid-filled system. The catheter is secured to the skull through an adjustable bolt, allowing placement at variable depths (up to 5 cm).
✔️The Codman Microsensor catheter can be used as an intraparenchymal or intraventricular monitor, depending on the depth of the catheter
✔️ Spiegelberg ICP monitors measure ICP through an air-pouch system attached to a pressure transducer connected to an electronic device. The probes differ, depending on where they rest (Epidural or Intraparenchymal)
🔸The incidence of infection ~ 2-7% with monitoring ≥ 5 days
🔸The risks are slightly greater with dural penetration
🔸The zero reference point of the transducer is usually taken as the external auditory meatus
🔸 Rather than the waveform type, the important factors appear to be the degree and duration of ICP elevation
🔸Two emerging non-invasive ICP monitoring methods include measuring the optic nerve sheath diameter (ONSD) as seen on an ultrasound probe placed on the superolateral aspect of the orbit and the pulsatility index (PI) which is cal- culated from transcranial Doppler studies (TCD).
#NeuroAnesthesia , #anaesthesia , #TheLayMedicalMan , #NeuroCriticalCare , #CriticalCare , #NeuroICU

ICTAL BRADYCARDIA AND ASYSTOLE : AN ENTITY ALL ANESTHESIOLOGISTS SHOULD KEEP IN MIND WHEN SEEING BRADYCARDIA IN A PATIENT WITH EPILEPSY

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📌Ictal bradycardia/asystole is a poorly recognised cause of collapse late in the course of a typical complex partial seizure

📌It is important to identify ictal bradycardia as a potential harbinger of lethal rhythms, such as asystole, as this may be one important mechanism leading to sudden unexpected death in epilepsy (SUDEP)
📌Tachycardia is the most common rhythm abnormality occurring in 64–100% of temporal lobe seizures. Ictal bradycardia has been reported in less than 6% of patients with complex partial seizures
📌The ictal bradycardia syndrome occurs in mostly in patients with temporal lobe seizures. 
📌It is believed that abnormal neuronal activity during a seizure can affect central autonomic regulatory centres in the brain leading to cardiac rhythm changes. 
📌Ictal bradycardia/asystole may be unrecognised until documented during video-electroencephalograph (video EEG)–electrocardiogram (ECG) monitoring in those with refractory epilepsy, often in the context of pre-surgical evaluation
📌Other rhythm abnormalities which can occur are change in heart rate variability, ictal tachycardias and atrioventricular (AV) block
📌If sufficiently severe, the ictal-induced bradyarrhythmia temporarily impairs both cerebral perfusion and cortical function; the result has the dual effect of terminating the seizure, while at the same time triggering syncope with consequent loss of consciousness and postural tone. In essence, a complex partial seizure patient may manifest both seizure and syncope features during the same episode.
📌There are currently no guidelines on who should undergo further cardiovascular investigations ; dual chamber pacemaker implantation has been suggested as a treatment in the long term, for epilepsy patients who manifest this syndrome and suffer repeated falls; but there is not much mention in literature both about diagnosis and about pharmacological and non pharmacological interventions to counter such episodes when presenting as an emergency situation in the perioperative scenario , especially when the patient is under anesthesia. 
#Neurology , #NeuroCriticalCare , #Anesthesia , #LayMedicalMan , #CriticalCare , #Epilepsy , #Cardiology , #CardiacAnesthesia
Reference: Ictal bradycardia and atrioventricular block: a cardiac manifestation of epilepsy; Salman S. Allana Hanna N. Ahmed Keval Shah Annie F. Kelly, Oxford Medical Case Reports, British Journal of Cardiology : Ictal Bradycardia and Asystole Associated with Intractable Epilepsy: A Case Series Elijah Chaila, Jaspreet Bhangu, Sandya Tirupathi, Norman Delanty; Ictal Asystole-Life-Threatening Vagal Storm or a Benign Seizure Self-Termination Mechanism? David G. Benditt, Gert van Dijk, Roland D. Thijs (Editorial:Circulation )

NORMAL SWALLOWING & DISORDERS OF SWALLOWING; For the #Neurologist & #NeuroCriticalCare #Physician

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  •   Cranial nerves V,VII,IX,X,XI,XII contributes
  •   2 brain stem nuclei control swallowing: (1) Nucleus Tractus Solitarius(NTS) which is a pure sensory nucleus in the medulla (2) Nucleus Ambiguous (NA) which is a motor nucleus situated deep in the reticular formation in medulla
  •   Sensory info sent via cranial nerves to NTS. Interneurons relay info to NA & surrounding reticular formation which sends efferent messages to cranial nerve pathways.
  •   Muscles innervated by Trigeminal nerve helps in Mastication, jaw closure, upward movement of larynx, backward movement of tongue to soft palate, tensing and elevation of soft palate and posterior pharyngeal wall constriction
  •   Muscles innervated by Facial nerve helps in mandibular depression and contributes to hyoid elevation
  •   Glossopharyngeal nerve supplies Stylopharyngeus , contributes to palatoglossus – portion of middle pharyngeal constrictor Ⓜ️NEMO> “Glossy nerve helps Stylish Middle Class”
  •   Vagus supplies muscles of soft palate (except Tensor Veli Palatini) – Superior, middle and inferior pharyngeal constrictors – Intrinsic muscles of larynx and muscles of esophagus Ⓜ️NEMO> “Vague nerve helps all classes”
  •   Recurrent Laryngeal Nerve innervates Cricopharyngeus muscle.
  •   Hypoglossal nerve innervates all intrinsic and some extrinsic muscles of tongue and geniohyoid ; hence responsible for all movements of the tongue
  •   Aetiology of swallowing disorders: Stroke, Traumatic Brain Injury, Brain Tumor , Cerebral Palsy, Neuroleptic drug- induced Tardive dyskinesia , Surgery ( Generally damage to the pharyngeal plexus may occur with anterior cervical fusion. Injury of the seventh, tenth, and twelfth cranial nerves may occur with carotid endarterectomy (as these nerves are close to the carotid bifurcation), various forms of dementia, Movement disorders including Parkinsons disease, Multiple Sclerosis , Amyotrophic Lateral Sclerosis (ALS)
  •   It has been suggested that recovery of swallowing in acute stroke patients may be rapid, warranting reassessment within 3 weeks of the initial swallowing evaluation
  •   Abnormal volitional cough, abnormal gag,dysarthria,dysphonia, cough after swallow, voice change after swallow are indicators of risk of aspiration after acute stroke
  •   But many of the neurologic disorders that affect swallowing are progressive; thus swallowing can be expected to decline as the disease worsens.
  •   Dysarthria may correlate with dysphagia with bulbar Amyotrophic Lateral Sclerosis (ALS). Dysphagia increases as respiratory capacity decreases regardless of the form of ALS. Vital capacity should be consistently measured, as accurate and timely assessment of a clinically relevant decline in respiratory status is crucial for determining the timing of feeding tube placement
  •   Pneumonia can be a frequent complication in patients with dysphagia owing to CNS disease
  •   Although an abnormal gag reflex may be apparent in patients with dysphagia resulting from various neurologic disorders, it may be absent in healthy control subjects or it may be normal in patients with neurogenic dysphagia
  •   The two imaging tools used to evaluate oropharyngeal dysphagia are Video Fluoroscopic Swallow Study (VSS- Gold Standard) and videoendoscopy. The Penetration-Aspiration Scale (PAS) provides an objective way during the VSS to measure the depth, response, and clearance of material entering the larynx and trachea.
  •   They are also valuable in identifying and teaching maneuvers that may facilitate swallowing and prevent aspiration in a patient.
  •   When significant aspiration cannot be prevented, alternatives to oral feeding such as percutaneous endoscopic gastrostomy (PEG) tube placement should be considered.
  •   Patients with oropharyngeal dysphagia owing to CNS lesions are best managed by a team approach including a speech pathologist, neurologist, and gastroenterologist.
  •   Swallowing therapy may include compensatory or rehabilitative strategies. Compensatory therapy does not change the physiology of the swallow; rather, bolus flow is redirected
  •   Compensatory strategies consist of manipulation of posture, consistency of the liquid, and sensory input. Facilitatory postures that have been studied in the neurogenic population include chin tuck and head rotation to the weak side 
  •   Rehabilitative therapy includes muscular strengthening and range of motion exercises, thermal-tactile application, and swallowing maneuvers
  •   Vocal fold medialization is the procedure generally performed to treat aspiration owing to an incompetent larynx
  •   A tracheotomy may be performed for neurologic patients with chronic aspiration. Although it does not improve swallowing, it facilitates pulmonary toileting
  •   Laryngotracheal separation is a more radical attempt to prevent chronic aspiration while allowing for oral intake. Although patients may return to oral diets, the ability to phonate is eliminated. If physiologic aspects of swallowing improve sufficiently, this procedure can be reversed, as the glottis is not affected.

#EPINEPHRINE ( #Adrenaline) : Pharmacological Highlights

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🔻Epinephrine is an agonist of alpha 1, β1 , and β2 adrenoceptors. An intravenous infusion of epinephrine produces an increase in mean arterial pressure (MAP) characterized by selectively enhanced systolic pressure with no change in diastolic pressure. 
🔻Epinephrine exerts positive chronotropic and inotropic actions by stimulation of β1 adrenoceptors

🔻Epinephrine also increases the rate of myocardial relaxation and enhances early LV filling, thereby improving diastolic function. These combined effects result in a dramatic increase in cardiac output.

🔻Epinephrine (0.01–0.03 ug kg –1 min –1 ) has been shown to produce similar hemodynamic effects with less pronounced tachycardia than dobutamine (2.5–5.0 ug kg–1 min–1 ) in patients after coronary artery bypass graft (CABG) surgery

🔻Predictable increase in cardiac output, favours the use of epinephrine as the primary inotropic drug for the management of LV dysfunction after cardiopulmonary bypass

🔻Epinephrine causes direct positive dromotropic effects ( leading to increase in conduction velocity and reduction of the refractory period of the AV node, His bundle, Purkinje fibers, and ventricular muscle)

🔻This may contribute to detrimental increases in ventricular rate in patients with atrial flutter or fibrillation and the occurrence of ventricular arrhythmias

🔻The overall effect of epinephrine on blood flow to a specific organ depends on the relative balance of alpha 1 and β2 adrenoceptors located in the vasculature.

🔻β2 -Adrenoceptors are sensitive to lower doses of epinephrine and, as a result, peripheral vasodilation and modest reductions in arterial pressure are observed with such doses

🔻In contrast, the effects of epinephrine on alpha 1 -adrenoceptors predominate at greater doses with marked increases in systemic vascular resistance and arterial pressure.

🔻The intense vasoconstriction produced by high doses of epinephrine may adversely impede LV ejection by increasing after load after cardiopulmonary bypass. Thus, greater doses of epinephrine may be used in combination with arterial vasodilators such as sodium nitroprusside to optimize contractile performance in such situations .

🔻Adrenaline via alpha 1 receptors also mediates (1) venoconstriction & enhanced venous return (2) Pulmonary vasoconstriction and increases in pulmonary arterial pressures.

🔻 Pre-existing β-blockade by nonselective β-blocker propranolol abolishes the decrease in systemic vascular resistance from epinephrine-induced stimulation of β2 adrenoceptors and potentiates peripheral vasoconstriction mediated by unopposed alpha 1 adrenoceptors.

🔻The positive inotropic and chronotropic effects of epinephrine are also attenuated in the presence of pre-existing β-blockade and greater doses of epinephrine are required to overcome this competitive blockade

🔻Complete pharmacologic blockade of β1 and β2 adrenoceptors may theoretically make the hemodynamic effects of epinephrine indistinguishable from those of the pure alpha 1 adrenoceptor agonist phenylephrine.

#NorAdrenaline , #CriticalCare , #vasopressors , #TheLayMedicalMan , #IntensiveCare , #Pharmacology, #anesthesia , #anaesthesia, #drugs

(Reference: Paul S. Pagel and David C. Warltier, Essential drugs in anesthesia practice Positive inotropic drugs, Anesthetic Pharmacology, 2nd edition)

JNC 8 GUIDELINES FOR MANAGEMENT OF SYSTEMIC HYPERTENSION 

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(1)📌In the general population aged 60 years or more , initiate pharmacologic treatment to lower blood pressure (BP) at systolic blood pressure (SBP) ≥150 mm Hg or diastolic blood pressure (DBP) ≥90 mm Hg and treat to a goal SBP <150 mm Hg and goal DBP <90 mm Hg

(2)📌In the general population aged ≥60 years, if pharmacologic treatment for high BP results in lower achieved SBP (eg, <140 mm Hg) and treatment is well tolerated and without adverse effects on health or quality of life, treatment does not need to be adjusted.
(3)📌In the general population <60 years, initiate pharmacologic treatment
(a) to lower BP at DBP ≥90mmHg and treat to a goal DBP <90mmHg.
(b) to lower BP at SBP ≥140 mm Hg and treat to a goal SBP <140 mm Hg.
(4)📌In the population aged ≥18 years with (i) diabetes & (ii) chronic kidney disease (CKD), initiate pharmacologic treatment to lower BP at SBP ≥140 mmHg or DBP ≥90 mmHg and treat to goal SBP <140mmHg and goal DBP <90mmHg.
(5)📌In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor

(ACEI), or angiotensin receptor blocker (ARB).
(6)📌In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB.
(7)📌In the population aged 18 years with CKD, initial (or add-on) antihypertensive treatment should include an ACEI or ARB to improve kidney outcomes. This applies to all CKD patients with hypertension regardless of race

or diabetes status.
(8)📌If goal BP is not reached within a month of treatment, increase the dose of the initial drug or add a second drug from one of the classes : thiazide-type diuretic, CCB,ACEI, or ARB. The clinician should continue to assess BP and adjust the treatment regimen until goal BP is reached.
(9)📌If goal BP cannot be reached with 2 drugs, add and titrate a third drug from the list mentioned above (). Do not use an ACEI and an ARB together in the same patient.
(10)📌If goal BP cannot be reached using only the drugs mentioned above, because of a contraindication or the need to use more than 3 drugs to reach goal BP, antihypertensive drugs from other classes can be used.
#hypertension , #medicine , #TheLayMedicalMan , #jnc8 , #HTN , #anesthesia , #pharmacology , #BloodPressure ,#BP