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myrawjcsmicasereports · 3 months ago

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Retinal and choroidal vascular drop out in a case of severe phenotype of Flammer Syndrome. Rescue of the ischemic-preconditioning mimicking action of endogenous Erythropoietin (EPO) by off-label intra vitreal injection of recombinant human EPO (rhEPO) by Claude Boscher in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: Erythropoietin (EPO) is a pleiotropic anti-apoptotic, neurotrophic, anti-inflammatory, and pro-angiogenic endogenous agent, in addition to its effect on erythropoiesis. Exogenous EPO is currently used notably in human spinal cord trauma, and pilot studies in ocular diseases have been reported. Its action has been shown in all (neurons, glia, retinal pigment epithelium, and endothelial) retinal cells. Patients affected by the Flammer Syndrome (FS) (secondary to Endothelin (ET)-related endothelial dysfunction) are exposed to ischemic accidents in the microcirculation, notably the retina and optic nerve.

Case Presentation: A 54 years old female patient with a diagnosis of venous occlusion OR since three weeks presented on March 3, 2019. A severe Flammer phenotype and underlying non arteritic ischemic optic neuropathy; retinal and choroidal drop-out were obviated. Investigation and follow-up were performed for 36 months with Retinal Multimodal Imaging (Visual field, SD-OCT, OCT- Angiography, Indo Cyanin Green Cine-Video Angiography). Recombinant human EPO (rhEPO)(EPREX®)(2000 units, 0.05 cc) off-label intravitreal injection was performed twice at one month interval. Visual acuity rapidly improved from 20/200 to 20/63 with disparition of the initial altitudinal scotoma after the first rhEPO injection, to 20/40 after the second injection, and gradually up to 20/32, by month 5 to month 36. Secondary cystoid macular edema developed ten days after the first injection, that was not treated via anti-VEGF therapy, and resolved after the second rhEPO injection. PR1 layer integrity, as well as protective macular gliosis were fully restored. Some level of ischemia persisted in the deep capillary plexus and at the optic disc.

Conclusion: Patients with FS are submitted to chronic ischemia and paroxystic ischemia/reperfusion injury that drive survival physiological adaptations via the hypoxic-preconditioning mimicking effect of endogenous EPO, that becomes overwhelmed in case of acute hypoxic stress threshold above resilience limits. Intra vitreal exogenous rhEPO injection restores retinal hypoxic-preconditioning adaptation capacity, provided it is timely administrated. Intra vitreal rhEPO might be beneficial in other retinal diseases of ischemic and inflammatory nature.

Key words : Erythropoietin, retinal vein occlusion, anterior ischemic optic neuropathy, Flammer syndrome, Primary Vascular Dysfunction, anti-VEGF therapy, Endothelin, microcirculation, off-label therapy.

Introduction

Retinal Venous Occlusion (RVO) treatment still carries insufficiencies and contradictions (1) due to the incomplete deciphering of the pathophysiology and of its complex multifactorial nature, with overlooking of factors other than VEGF up-regulation, notably the roles of retinal venous tone and Endothelin-1 (ET) (2-5), and of endothelial caspase-9 activation (6). Flammer Syndrome (FS)( (Primary Vascular Dysfunction) is related to a non atherosclerotic ET-related endothelial dysfunction in a context of frequent hypotension and increased oxidative stress (OS), that alienates organs perfusion, with notably changeable functional altered regulation of blood flow (7-9), but the pathophysiology remains uncompletely elucidated (8). FS is more frequent in females, and does not seem to be expressed among outdoors workers, implying an influence of sex hormons and light (7)(9). ET is the most potent pro-proliferative, pro-fibrotic, pro-oxidative and pro-inflammatory vasoconstrictor, currently considered involved in many diseases other than cardio-vascular ones, and is notably an inducer of neuronal apoptosis (10). It is produced by endothelial (EC), smooth vascular muscles (SVMC) and kidney medullar cells, and binds the surface Receptors ET-A on SVMC and ET-B on EC, in an autocrine and paracrine fashion. Schematically, binding on SVMC Receptors (i.e. through local diffusion in fenestrated capillaries or dysfunctioning EC) and on EC ones (i.e. by circulating ET) induce respectively arterial and venous vasoconstriction, and vasodilation, the latter via Nitrite oxide (NO) synthesis. ET production is stimulated notably by Angiotensin 2, insulin, cortisol, hypoxia, and antagonized by endothelial gaseous NO, itself induced by flow shear stress. Schematically but not exclusively, vascular tone is maintained by a complex regulation of ET-NO balance (8) (10-11). Both decrease of NO and increase of ET production are both a cause and consequence of inflammation, OS and endothelial dysfunction, that accordingly favour vasoconstriction; in addition ET competes for L-arginine substrate with NO synthase, thereby reducing NO bioavailability, a mechanism obviated notably in carotid plaques and amaurosis fugax (reviewed in 11).

Severe FS phenotypes are rare. Within the eye, circulating ET reaches retinal VSMC in case of Blood-Retinal-Barrier (BRB) rupture and diffuses freely via the fenestrated choroidal circulation, notably around the optic nerve (ON) head behind the lamina cribrosa, and may induce all pathologies related to acute ocular blood flow decrease (2-3)(5)(7-9). We previously reported two severe cases with rapid onset of monocular cecity and low vision, of respectively RVO in altitude and non arteritic ischemic optic neuropathy (NAION) (Boscher et al, Société Francaise d'Ophtalmologie and Retina Society, 2015 annual meetings).

Exogenous Recombinant human EPO (rhEPO) has been shown effective in humans for spinal cord injury (12), neurodegenerative and chronic kidney diseases (CKD) (reviewed in 13). Endogenous EPO is released physiologically in the circulation by the kidney and liver; it may be secreted in addition by all cells in response to hypoxic stress, and it is the prevailing pathway induced via genes up-regulation by the transcription factor Hypoxia Inducible Factor 1 alpha, among angiogenesis (VEGF pathway), vasomotor regulation (inducible NO synthase), antioxidation, and energy metabolism (14). EPO Receptor signaling induces cell proliferation, survival and differentiation (reviewed in 13), and targets multiple non hematopoietic pathways as well as the long-known effect on erythropoiesis (reviewed in 15). Of particular interest here, are its synergistic anti-inflammatory, neural antiapoptotic (16) pro-survival and pro-regenerative (17) actions upon hypoxic injury, that were long-suggested to be also indirect, via blockade of ET release by astrocytes, and assimilated to ET-A blockers action (18). Quite interestingly, endogenous EPO’s pleiotropic effects were long-summarized (back to 2002), as “mimicking hypoxic-preconditioning” by Dawson (19), a concept applied to the retina (20). EPO Receptors are present in all retinal cells and their rescue activation targets all retinal cells, i.e. retinal EC, neurons (photoreceptors (PR), ganglion (RGG) and bipolar cells), retinal pigment epithelium (RPE) osmotic function through restoration of the BRB, and glial cells (reviewed in 21), and the optic nerve (reviewed in 22). RhEPO has been tested experimentally in animal models of glaucoma, retinal ischemia-reperfusion (I/R) and light phototoxicity, via multiple routes (systemic, subconjunctival, retrobulbar and intravitreal injection (IVI) (reviewed in 23), and used successfully via IVI in human pilot studies, notably first in diabetic macular edema (24) (reviewed in 25 and 26). It failed to improve neuroprotection in association to corticosteroids in optic neuritis, likely for bias reasons (reviewed in 22). Of specific relation to the current case, it has been reported in NAION (27) (reviewed in 28) and traumatic ON injury (29 Rashad), and in one case of acute severe central RVO (CRVO) (Luscan and Roche, Société Francaise d’Ophtalmologie 2017 annual meeting). In addition EPO RPE gene therapy was recently suggested to prevent retinal degeneration induced by OS in a rodent model of dry Age Macular Degeneration (AMD) (30).

Case Report Presentation

This 54 years female patient was first visited on March 2019 4th, seeking for second opinion for ongoing vision deterioration OR on a daily basis, since around 3 weeks. Sub-central RVO (CRVO) OR had been diagnosed on February 27th; available SD-OCT macular volume was increased with epiretinal marked hyperreflectivity, one available Fluorescein angiography picture showed a non-filled superior CRVO, and a vast central ischemia involving the macular and paraoptic territories. Of note there was ON edema with a para-papillary hemorrage nasal to the disc on the available colour fundus picture.

At presentation on March 4, Best Corrected Visual Acuity (BCVA) was reduced at 20/100 OR (20/25 OS). The patient described periods of acutely excruciating retro-orbital pain in the OR. Intraocular pressure was normal, at 12 OR and 18 OS (pachymetry was at 490 microns in both eyes). The dilated fundus examination was similar to the previous color picture and did not disclose peripheral hemorrages recalling extended peripheral retinal ischemia. Humphrey Visual Field disclosed an altitudinal inferior scotoma and a peripheral inferior scotoma OR and was in the normal range OS, i.e. did not recall normal tension glaucoma OS . There were no papillary drusen on the autofluorescence picture, ON volume was increased (11.77 mm3 OR versus 5.75 OS) on SD-OCT (Heidelberg Engineering®) OR, Retinal Nerve Fiber (RNFL) and RGC layers thicknesses were normal Marked epimacular hypereflectivity OR with foveolar depression inversion, moderately increased total volume and central foveolar thickness (CFT) (428 microns versus 328 OS), and a whitish aspect of the supero-temporal internal retinal layers recalling ischemic edema, were present . EDI CFT was incresead at 315 microns (versus 273 microns OS), with focal pachyvessels on the video mapping . OCT-Angiography disclosed focal perfusion defects in both the retinal and chorio-capillaris circulations , and central alterations of the PR1 layer on en-face OCT

Altogether the clinical picture evoked a NAION with venous sub-occlusion, recalling Fraenkel’s et al early hypothesis of an ET interstitial diffusion-related venous vasoconstriction behind the lamina cribrosa (2), as much as a rupture of the BRB was present in the optic nerve area (hemorrage along the optic disc). Choroidal vascular drop-out was suggested by the severity and rapidity of the VF impairment (31). The extremely rapid development of a significant “epiretinal membrane”, that we interpreted as a reactive - and protective, in absence of cystoid macular edema (CME) - ET 2-induced astrocytic proliferation (reviewed in 32), was as an additional sign of severe ischemia.

The mention of the retro-orbital pain evoking a “ciliary angor”, the absence of any inflammatory syndrome and of the usual metabolic syndrome in the emergency blood test, oriented the etiology towards a FS. And indeed anamnesis collected many features of the FS, i.e. hypotension (“non dipper” profile with one symptomatic nocturnal episode of hypotension on the MAPA), migrains, hypersensitivity to cold, stress, noise, smells, and medicines, history of a spontaneously resolutive hydrops six months earlier, and of paroxystic episods of vertigo (which had driven a prior negative brain RMI investigation for Multiple Sclerosis, a frequent record among FS patients (33) and of paroxystic visual field alterations (7)(9), that were actually recorded several times along the follow-up.

The diagnosis of FS was eventually confirmed in the Ophthalmology Department in Basel University on April 10th, with elevated retinal venous pressure (20 to 25mmHg versus 10-15 OS) (4)(7)(9), reduced perfusion in the central retinal artery and veins on ocular Doppler (respectively 8.3 cm/second OR velocity versus 14.1 mmHg OS, and 3.1/second OR versus 5.9 cm OS), and impaired vasodilation upon flicker light-dependant shear stress on the Dynamic Vessel Analyser testing (7-9). In addition atherosclerotic plaques were absent on carotid Doppler.

On March 4th, the patient was at length informed about the FS, a possible off label rhEPO IVI, and a related written informed consent on the ratio risk-benefits was delivered.

By March 7th, she returned on an emergency basis because of vision worsening OR. VA was unchanged, intraocular pressure was at 13, but Visual Field showed a worsening of the central and inferior scotomas with a decreased foveolar threshold, from 33 to 29 decibels. SD-OCT showed a 10% increase in the CFT volume.

On the very same day, an off label rhEPO IVI OR (EPREX® 2000 units, 0,05 cc in a pre-filled syringe) was performed in the operating theater, i.e. the dose reported by Modarres et al (27), and twenty times inferior to the usual weekly intravenous dose for treatment of chronic anemia secondary to CKD. Intra venous acetazolamide (500 milligrams) was performed prior to the injection, to prevent any increase in intra-ocular pressure. The patient was discharged with a prescription of chlorydrate betaxolol (Betoptic® 0.5 %) two drops a day, and high dose daily magnesium supplementation (600 mgr).

Incidentally the patient developed bradycardia the day after, after altogether instillation of 4 drops of betaxolol only, that was replaced by acetazolamide drops, i.e. a typical hypersensitivity reaction to medications in the FS (7)(9).

Subjective vision improvement was recorded as early as D1 after injection. By March 18 th, eleven days post rhEPO IVI, BCVA was improved at 20/63, the altitudinal scotoma had resolved (Fig. 5), Posterior Vitreous Detachment had developed with a disturbing marked Weiss ring, optic disc swelling had decreased; vasculogenesis within the retinal plexi and some regression of PR1 alterations were visible on OCT-en face. Indeed by 11 days post EPO significant functional, neuronal and vascular rescue were observed, while the natural evolution had been seriously vision threatening.

However cystoid ME (CME) had developed . Indo Cyanin Green-Cine Video Angiography (ICG-CVA) OR, performed on March 23, i.e. 16 days after the rhEPO IVI, showed a persistent drop in ocular perfusion: ciliary and central retinal artery perfusion timings were dramatically delayed at respectively 21 and 25 seconds, central retinal vein perfusion initiated by 35 seconds, was pulsatile, and completed by 50 seconds only (video 3). Choroidal pachyveins matching the ones on SD-OCT video mapping were present in the temporal superior and inferior fields, and crossed the macula; capillary exclusion territories were present in the macula and around the optic disc.

By April 1, 23 days after the rhEPO injection, VA was unchanged, but CME and perfusion voids in the superficial deep capillary plexi and choriocapillaris were worsened, and optic disc swelling had recurred back to baseline, in a context of repeated episodes of systemic hypotension; and actually Nifepidin-Ratiopharm® oral drops (34), that had been delivered via a Temporary Use Authorization from the central Pharmacology Department in Assistance Publique Hopitaux de Paris, had had to be stopped because of hypersensitivity.

A second off label rhEPO IVI was performed in the same conditions on April 3, i.e. approximately one month after the first one.

Evolution was favourable as early as the day after EPO injection 2: VA was improved at 20/40, CME was reduced, and perfusion improved in the superficial retinal plexus as well as in the choriocapillaris. By week 4 after EPO injection 2, CME was much decreased, i.e. without anti VEGF injection. On august 19th, by week 18 after EPO 2, perfusion on ICG-CVA was greatly improved , with ciliary timing at 18 seconds, central retinal artery at 20 seconds and venous return from 23 to 36 seconds, still pulsatile. Capillary exclusion territories were visible in the macula and temporal to the macula after the capillary flood time that went on by 20.5 until 22.5 seconds (video 4); they were no longer persistent at intermediate and late timings.

Last complete follow-up was recorded on January 7, 2021, at 22 months from EPO injection 2. BCVA was at 20/40, ON volume had dropped at 7.46 mm3, a sequaelar superior deficit was present in the RNFL with some corresponding residual defects on the inferior para central Visual Field , CFT was at 384 mm3 with an epimacular hyperreflectivity without ME, EDI CFT was dropped at 230 microns. Perfusion on ICG-CVA was not normalized, but even more improved, with ciliary timing at 15 seconds, central retinal artery at 16 seconds and venous return from 22 to 31 seconds, still pulsatile , indicating that VP was still above IOP. OCT-A showed persisting perfusion voids, especially at the optic disc and within the deep retinal capillary plexus. The latter were present at some degree in the OS as well . Choriocapillaris and PR1 layer were dramatically improved.

Last recorded BCVA was at 20/32 by February 14, 2022, at 34 months from EPO 2. SD-OCT showed stable gliosis hypertrophy and mild alterations of the external layers .

Discussion

What was striking in the initial clinical phenotype of CRVO was the contrast between the moderate venous dilation, and the intensity of ischemia, that were illustrating the pioneer hypothesis of Professor Flammer‘s team regarding the pivotal role of ET in VO (2), recently confirmed (3)(35), i.e. the local venous constriction backwards the lamina cribrosa, induced by diffusion of ET-1 within the vascular interstitium, in reaction to hypoxia. NAION was actually the primary and prevailing alteration, and ocular hypoperfusion was confirmed via ICG-CVA, as well as by the ocular Doppler performed in Basel. ICG-CVA confirmed the choroidal drop-out suggested by the severity of the VF impairment (31) and by OCT-A in the choriocapillaris. Venous pressure measurement, which instrumentation is now available (8), should become part of routine eye examination in case of RVO, as it is key to guide cases analysis and personalized therapeutical options.

Indeed, the endogenous EPO pathway is the dominant one activated by hypoxia and is synergetic with the VEGF pathway, and coherently it is expressed along to VEGF in the vitreous in human RVO (36). Diseases develop when the individual limiting stress threshold for efficient adaptative reactive capacity gets overwhelmed. In this case by Week 3 after symtoms onset, neuronal and vascular resilience mechanisms were no longer operative, but the BRB, compromised at the ON, was still maintained in the retina.

As mentioned in the introduction, the scientific rationale for the use of EPO was well demonstrated by that time, as well as the capacities of exogenous EPO to mimic endogenous EPO vasculogenesis, neurogenesis and synaptogenesis, restoration of the balance between ET-1 and NO. Improvement of chorioretinal blood flow was actually illustrated by the evolution of the choriocapillaris perfusion on repeated OCT-A and ICG-CVA. The anti-apoptotic effect of EPO (16) seems as much appropriate in case of RVO as the caspase-9 activation is possibly another overlooked co-factor (6).

All the conditions for translation into off label clinical use were present: severe vision loss with daily worsening and unlikely spontaneous favourable evolution, absence of toxicity in the human pilot studies, of contradictory comorbidities and co-medications, and of context of intraocular neovascularization that might be exacerbated by EPO (37).

Why didn’t we treat the onset of CME by March 18th, i.e. eleven days after EPO IVI 1, by anti-VEGF therapy, the “standard-of-care” in CME for RVO ?

In addition to the context of functional, neuronal and vascular improvements obviated by rhEPO IVI by that timing in the present case, actually anti VEGF therapy does not address the underlying causative pathology. Coherently, anti-VEGF IVI : 1) may not be efficient in improving vision in RVO, despite its efficiency in resolving/improving CME (usually requiring repeated injections), as shown in the Retain study (56% of eyes with resolved ME continued to loose vision)(quoted in (1) 2) eventually may be followed by serum ET-1 levels increase and VA reduction (in 25% of cases in a series of twenty eyes with BRVO) (38) and by increased areas of non perfusion in OCT-A (39). Rather did we perform a second hrEPO IVI, and actually we consider open the question whether the perfusion improvement, that was progressive, might have been accelerated/improved via repeated rhEPO IVI, on a three to four weeks basis.

The development of CME itself, involving a breakdown of the BRB, i.e. of part of the complex retinal armentorium resilience to hypoxia, was somewhat paradoxical in the context of improvement after the first EPO injection, as EPO restores the BRB (24), and as much as it was suggested that EPO inhibits glial osmotic swelling, one cause of ME, via VEGF induction (40). Possible explanations were: 1) the vascular hyperpermeability induced by the up-regulation of VEGF gene expression via EPO (41) 2) the ongoing causative disease, of chronic nature, that was obviated by the ICG-CVA and the Basel investigation, responsible for overwhelming the gliosis-dependant capacity of resilience to hypoxia 3) a combination of both. I/R seemed excluded: EPO precisely mimics hypoxic reconditioning as shown in over ten years publications, including in the retina (20), and as EPO therapy is part of the current strategy for stabilization of the endothelial glycocalix against I/R injury (42-43). An additional and not exclusive possible explanation was the potential antagonist action of EPO on GFAP astrocytes proliferation, as mentioned in the introduction (18), that might have counteracted the reactive protective hypertrophic gliosis, still fully operative prior to EPO injection, and that was eventually restored during the follow-up, where epiretinal hyperreflectivity without ME and ongoing chronic ischemia do coincide (Fig. 6 and video 6), as much as it is unlikely that EPO’s effect would exceed one month (cf infra). Inhibition of gliosis by EPO IVI might have been also part of the mechanism of rescue of RGG, compromised by gliosis in hypoxic conditions (44). Whatever the complex balance initially reached, then overwhelmed after EPO IVI 1, the challenge was rapidly overcome by the second EPO IVI without anti-VEGF injection, likely because the former was powerful enough to restore the threshold limit for resilience to hypoxia, that seemed no longer reached again during the relapse-free follow-up. Of note, this “epiretinal membrane “, which association to good vision is a proof of concept of its protective effect, must not be removed surgically, as it would suppress one of the mecanisms of resilience to hypoxia.

To our best knowledge, ICG-CVA was never reported in FS; it allows real time evaluation of the ocular perfusion and illustration of the universal rheological laws that control choroidal blood flow as well. Pachyveins recall a “reverse” veno-arteriolar reflex in the choroidal circulation, that is NO and autonomous nervous system-dependant, and that we suggested to be an adaptative choroidal microcirculation process to hypoxia (45). Their persistence during follow-up accounts for a persisting state of chronic ischemia.

The optimal timing for reperfusion via rhEPO in a non resolved issue:

in the case reported by Luscan and Roche, rhEPO IVI was performed on the very same day of disease onset, where it induced complete recovery from VA reduced at counting fingers at 1 meter, within 48 hours. This clinical human finding is on line with a recent rodent stroke study that established the timings for non lethal versus lethal ischemia of the neural and vascular lineages, and the optimized ones for beneficial reperfusion: the acute phase - from Day 1 where endothelial and neural cells are still preserved, to Day 7 where proliferation of pericytes and Progenitor Stem Cells are obtainable - and the chronic stage, up to Day 56, where vasculogenesis, neurogenesis and functional recovery are still possible, but with uncertain efficiency (46). In our particular case, PR rescue after rhEPO IVI 1 indicated that Week 3 was still timely. RhEPO IVI efficacy was shown to last between one (restoration of the BRB) and four weeks (antiapoptotic effect) in diabetic rats (24). The relapse after Week 3 post IVI 1 might indicate that it might be approximately the interval to be followed, should repeated injections be necessary.

The bilateral chronic perfusion defects on OCT-A at last follow-up indicate that both eyes remain in a condition of chronic ischemia and I/R, where endogenous EPO provides efficient ischemic pre-conditioning, but is potentially susceptible to be challenged during episodes of acute hypoxia that overwhelm the resilience threshold.

Conclusion

The present case advocates for individualized medicine with careful recording of the medical history, investigation of the systemic context, and exploiting of the available retinal multimodal imaging for accurate analytical interpretation of retinal diseases and their complex pathophysiology. The Flammer Syndrome is unfortunately overlooked in case of RVO; it should be suspected clinically in case of absence of the usual vascular and metabolic context, and in case of elevated RVP. RhEPO therapy is able to restore the beneficial endogenous EPO ischemic pre-conditioning in eyes submitted to challenging acute hypoxia episodes in addition to chronic ischemic stress, as in the Flammer Syndrome and fluctuating ocular blood flow, when it becomes compromised by the overwhelming of the hypoxic stress resilience threshold. The latter physiopathological explanation illuminates the cases of RVO where anti-VEGF therapy proved functionally inefficient, and/or worsened retinal ischemia. RhEPO therapy might be applied to other chronic ischemia and I/R conditions, as non neo-vascular Age Macular Degeneration (AMD), and actually EPO was listed in 2020 among the nineteen promising molecules in AMD in a pooling of four thousands (47).

#off-label therapy #JCRMHS #anti-VEGF therapy #Erythropoietin #Journal of Clinical Case Reports Medical Images and Health Sciences impact factor.#Primary Vascular Dysfunction

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san-myshuno-er · 2 years ago

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Shawn: Alright, here we go! Let's get this gentleman to Trauma 2.

Cam Landry: What's your name, Sir? Sir, can you tell me your name?

Patient: It's Wilson.

Shawn: Okay, Mr. Wilson, I'm Dr. Jones, this is Nurse Cam, and we're going to take very good care of you.

Mike Davis: What's your name, sir?

Patient: It's Canelli. George Canelli.

Paramedic: Suspected MI, 500cc of Saline are in. Slight head trauma, he must have hit his head on the steering wheel.

Quinn: Alright, Mr Canelli. I'm Dr. Roe, let's get you down to Trauma 1.

Mr Canelli: Could someone perhaps call my son and daughter? I was... (heavy breathing) on my way to my son's house to see my grandchildren...

Quinn: Of course. Why don't you give the number to Nurse Mike here, he'll see to it.

Mr Canelli: (chuckles) men are nurses, and women are doctors...

Quinn: It's a changed world, sir.

Quinn: Alright, let's have a listen.

Mike: Pulse Ox is 97, BP is 117 to 87. Pulse is 135.

Mr. Canelli: That's not so bad, is it, Doctor?

Quinn: Sir, if you speak I can't hear your heart. I hear some crackling there. Let's get a EKG, CBC, Chem-7-

Mr. Canelli: What's that?

Quinn: Some blood tests, we look for your blood urea nitrogen, carbon dioxide, creatinine, glucose, chloride, potassium, and sodium values. Other than that, I want cardiac enzymes and, just to be safe, a cross table head and chest X-Ray. Once we get those back, we'll know more.

Mike: First saline is in.

Quinn: Good. Let's see what those tests say.

Shawn: Okay, let's have a looksie. Lights, please! Oh wow. Have some nice and pleasant thoughts, sir. (to the nurses) Let's have a CBC, type and cross-match. We got a pre-op here... Notify the OR, we need a room.

Cam: It's not completely severed, is it?

Shawn: No... still some attachment left. That's a good sign, sir.

Shawn: Call Vascular and Orthopedic. Tell them to get down here right now. This is their lucky day! Mr. Wilson, your hand is barely attached, but it's gonna be okay. Get me an EKG and an X-Ray of his wrist and hand... can you feel anything in your hand?

Mr. Wilson: No...

Shawn: We'll save your hand, don't worry.

Quinn: Mr. Canelli, we are going to call Cardiology as soon as those tests are back, and then they can decide what kind of treatment you might need.

Mike: Quinn, pulse ox and pressure are going down!

Quinn: I'm losing his pulse; Mr Canelli? Mr Canelli?!

Previous | Beginning | Next

(sorry this post took so long!! real life got into the way...)

#simblr #the sims #the sims 4 #ts4 #s4 #sims 4 story #sims 4 screenshots #ts4 story #san myshuno er #sm er #ts4 gameplay #new blog #new simblr #smerSim: Quinn #smersim: shawn #smerSim: Mike #smerSim: Cam

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a-forbidden-detective · 2 years ago

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Just when I think the story’s end is near… Akira pulls out this stunt that makes me want to scream!

Neck injuries constitute a lot of organs that can be harmed (total carotid arteries and internal junial veins, larynx, trachea, esophagus, thyroid and various nerves), so this is quite alarming if Ron not only damaged his vocal cords.

Assuming that he is knowledgeable of anatomy like he should be as a Holmes/Moriarty descendant, Ron stabbing his neck is worrying.

Penetrating neck injuries are life-threatening emergencies. The ATLS guidelines outline the initial management of neck trauma patients. Airway management is the first action, if the patient has no significant vascular injury. All patients who have penetrating neck trauma should be examined periodically for hematoma or edema of the neck. Voice quality and airway patency might be improved if laryngeal repair is performed within 24 hours of trauma. CT angiography should be performed for all neck penetration patients whose injuries penetrate the platysma. CT might be helpful for diagnosing laryngeal fractures in intubated patients. A patient who has a neck injury should be admitted and monitored for 24 hours after surgical treatment. This could prevent morbidity or mortality from hemorrhage or respiratory distress. If possible, the injured laryngeal tissues should be preserved and not sacrificed.

Because of it I am forced to look at the health journals online. (Click at your own risk as it can get a little graphic on the descriptions.) I’d like to know the potential damage it would cause if he didn’t get an immediate medical attention.

This is Ron’s Reichenbach Fall.

#akira amano #ron kamonohashi #kamonohashi ron no kindan suiri #rkdd spoilers #totomaru isshiki #deranged detective #milo moriarty #ron et toto #ron kamonohashi: deranged detective #rkdd

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universitypenguin · 10 months ago

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I’ve worked in a trauma center long enough to have seen someone get stabbed directly in the heart and still survive because of how quickly they were treated. Even if an artery is cut, tourniquets and a vascular surgeon can work wonders. There’s literally like four or five places on the body that could result in an injury serious enough to kill someone (assuming they had prompt access to first aide and got treatment for the wound in a reasonable timeframe.) A portion of people who are stabbed in those vulnerable places do end up with life altering physical damage, but they still survive.

Writers who are looking to make their stories realistic should be aware of this, but it’s not common knowledge outside of the medical field.

one of my greatest pet peeves in fiction, and it is truly stupid I know, is that no one seems to understand how genuinely hard it is to kill someone via stabbing. stab wounds have a mortality rate of like 5%. especially abdominal stabbing. tv shows and movies show dudes getting stabbed one time in the lower abdomen with a tiny knife and then they fall over. like what did he die of precisely. that man died of Small Knife

#so true #it often just goes into muscle #or into the peritoneal cavity #if you hit an artery that’s different #but surviving that is definitely possible #if you apply a torniquet and get them to a vascular surgeon #they’ll probably make it #plus your really essential organs are well protected

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drlalitbhardwaj · 7 days ago

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Advanced Surgical Techniques: Dr. Bhardwaj uses the latest advancements in neurosurgery to ensure minimally invasive procedures whenever possible. This reduces recovery time and lowers the risk of complications, giving patients a better chance at a full recovery.

Personalized Care: Every patient’s condition is unique. Dr. Bhardwaj takes a personalized approach, carefully assessing each case and developing a treatment plan that best suits the individual’s needs. He ensures that his patients and their families are well-informed throughout the entire process.

Comprehensive Treatment: From the initial consultation and diagnosis to post-surgery recovery and rehabilitation, Dr. Bhardwaj offers comprehensive care. His holistic approach ensures that patients receive the support they need at every stage of treatment.

Patient Satisfaction and Recovery: Dr. Bhardwaj’s commitment to his patients is evident in the success stories of many individuals who have undergone brain hemorrhage surgery under his care. His patients often praise his dedication, attention to detail, and the compassionate manner in which he addresses their concerns.

The Importance of Timely Treatment

The sooner a brain hemorrhage is diagnosed and treated, the better the chances of a successful recovery. Delayed treatment can lead to brain damage, disability, or even death. This is why it is critical to seek the help of a Brain Hemorrhage Surgeon in Jaipur like Dr. Lalit Bhardwaj at the first sign of any neurological issues.

Whether it’s a sudden, severe headache, weakness, vision changes, or difficulty speaking, seeking immediate medical advice can make all the difference. Dr. Bhardwaj’s expertise ensures that your condition is managed efficiently and effectively, with the goal of minimizing damage and improving your quality of life.

Conclusion

Dr. Lalit Bhardwaj is a trusted and skilled Brain Hemorrhage Surgeon in Jaipur who provides high-quality, compassionate care to patients with brain hemorrhage and other neurological conditions. His dedication to using advanced techniques and delivering personalized treatment plans has made him one of the top choices for neurosurgery in Jaipur.

If you or a loved one is dealing with a brain hemorrhage or any neurological condition, don’t wait for the symptoms to worsen. Consult with Dr. Lalit Bhardwaj, a leading Brain Hemorrhage Surgeon in Jaipur, and take the first step towards recovery. Your brain health deserves the best care available — trust Dr. Bhardwaj to provide it.

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earlystagediabeticfootulcers · 7 days ago

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Early Stage Diabetic Foot Ulcers: A Call to Action for Early Diagnosis and Management

Diabetes mellitus is a chronic metabolic condition that affects millions worldwide, with India bearing a significant burden. One of the most concerning complications of diabetes is diabetic foot ulcers (DFUs), which pose a severe threat to mobility and overall quality of life. Early-stage diabetic foot ulcers (DFUs) are a critical yet often overlooked phase of this condition. Addressing them at the earliest stage can significantly reduce complications, improve patient outcomes, and lower healthcare costs.

Understanding Early-Stage Diabetic Foot Ulcers

Early-stage diabetic foot ulcers are superficial, non-infected wounds primarily affecting the skin’s outermost layers. They are often the result of repetitive trauma, poor glycemic control, and underlying neuropathy or vascular compromise. Identifying and addressing these ulcers early can prevent progression to deeper, infected, or gangrenous wounds that may require invasive interventions.

Key Features of Early-Stage DFUs:

Redness or discoloration of the affected area.

Superficial breaks in the skin with minimal discharge.

Absence of systemic infection or deep tissue involvement.

Associated neuropathy leading to reduced pain perception.

Risk Factors for Early-Stage DFUs

Peripheral Neuropathy: Reduced sensation increases the likelihood of unnoticed trauma.

Peripheral Arterial Disease (PAD): Compromised blood flow delays wound healing.

Hyperglycemia: Prolonged high blood sugar levels impair immune function and tissue repair.

Improper Footwear: Shoes that cause pressure points or friction.

Poor Foot Hygiene: Increased risk of infection and skin breakdown.

Importance of Early Diagnosis

Timely identification of early-stage DFUs is essential to prevent complications. Screening for neuropathy, vascular insufficiency, and skin integrity should be a routine practice for individuals with diabetes. Vascular specialists play a pivotal role in assessing arterial health through non-invasive techniques like ankle-brachial index (ABI) and Doppler studies.

Management Strategies for Early-Stage DFUs

Glycemic Control: Maintaining blood sugar levels within target ranges promotes effective wound healing and reduces the risk of infection.

Wound Care:

Regular cleansing with sterile solutions.

Application of non-adherent, moist wound dressings.

Debridement of calluses and necrotic tissue as needed.

Pressure Offloading: Using custom orthotics or offloading devices to reduce pressure on the ulcerated area.

Infection Prevention:

Use of topical antibiotics for superficial infections.

Close monitoring for signs of systemic infection.

Vascular Health Optimization:

Addressing PAD with pharmacological or interventional treatments.

Ensuring adequate circulation to promote healing.

Preventive Measures

Routine Foot Exams: Patients with diabetes should inspect their feet daily and undergo regular professional foot evaluations.

Education on Foot Care:

Proper cleaning and moisturizing of feet.

Avoiding barefoot walking.

Appropriate Footwear: Shoes should provide cushioning and prevent pressure points.

Regular Vascular Assessments: Periodic evaluation of arterial health, especially for those with a history of PAD or ulcers.

The Role of Multidisciplinary Care

Managing early-stage diabetic foot ulcers requires a coordinated approach involving diabetologists, vascular surgeons, podiatrists, and wound care specialists. Early referral to vascular specialists is crucial for patients with signs of compromised circulation or non-healing wounds.

Conclusion

Early-stage diabetic foot ulcers present an opportunity for intervention before complications arise. Proactive measures, including education, regular screenings, and timely treatment, are essential to curb the progression of DFUs. The Vascular Society of India is uniquely positioned to lead efforts in raising awareness, promoting research, and developing clinical guidelines to improve the lives of patients living with diabetes and its complications.

#dibetic foot ulcers #foot ulcers

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drsaurabhjaiswal12 · 11 days ago

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Dr. Saurabh Jaiswal — The Best CTVS Surgeon for Heart Surgery in Jaipur

When it comes to heart surgery, choosing the right surgeon is paramount to ensure the best possible outcome. Dr. Saurabh Jaiswal, a renowned CTVS surgeon in Jaipur, stands out as one of the most skilled and experienced specialists in cardiac surgery. With a reputation for excellence, Dr. Jaiswal has helped countless patients lead healthier lives after undergoing various complex heart procedures, including Minimally Invasive Heart Surgery in Jaipur.

Expertise and Qualifications

Dr. Saurabh Jaiswal is a highly qualified Cardiothoracic and Vascular Surgeon (CTVS) with extensive training in the latest techniques for heart surgery. His educational background includes prestigious medical degrees, extensive hands-on experience in both national and international settings, and continuous professional development to stay ahead of innovations in cardiac care.

Minimally Invasive Heart Surgery in Jaipur

One of the most remarkable advancements in heart surgery is Minimally Invasive Heart Surgery, and Dr. Saurabh Jaiswal is a pioneer in bringing this innovative technique to Jaipur. Minimally invasive surgery involves smaller incisions compared to traditional open-heart surgery, which leads to several benefits for the patient, including:

Shorter Recovery Time: With smaller incisions and less trauma to the body, patients typically experience a quicker recovery, often allowing them to return to their normal activities much sooner than with conventional heart surgery.

Reduced Risk of Infection: Smaller incisions mean less exposure to the external environment, reducing the chances of post-surgical infections and complications.

Less Pain and Scarring: The smaller the incision, the less pain and scarring a patient will experience. This significantly improves the patient’s post-operative comfort.

Improved Aesthetic Results: Because the incisions are smaller and placed in less visible areas, patients enjoy better aesthetic results with less noticeable scarring.

Dr. Jaiswal’s expertise in Minimally Invasive Heart Surgery in Jaipur makes him a leader in the field, offering patients an option for heart surgery that is less invasive but just as effective. Whether you are dealing with coronary artery disease, valve diseases, or other heart conditions, this advanced approach can significantly improve your recovery experience and overall outcomes.

Comprehensive Heart Care

Dr. Saurabh Jaiswal doesn’t just perform surgeries — he provides comprehensive heart care. From the initial diagnosis to post-operative care, he ensures that every patient receives personalized treatment based on their unique needs. His approach is built on thorough assessments, advanced diagnostics, and cutting-edge treatment options that deliver superior results.

He specializes in treating conditions such as:

Coronary Artery Disease (CAD)

Congenital Heart Defects

Heart Valve Diseases (Stenosis, Regurgitation)

Aortic Aneurysms

Arrhythmias and other heart conditions

His multidisciplinary approach ensures that all aspects of a patient’s heart health are addressed, ensuring the most effective and tailored treatment.

Why Choose Dr. Saurabh Jaiswal for Your Heart Surgery?

When it comes to heart surgery, particularly Minimally Invasive Heart Surgery in Jaipur, Dr. Saurabh Jaiswal offers a combination of unmatched skill, cutting-edge technology, and a compassionate approach to patient care. Here’s why Dr. Jaiswal is considered one of the best cardiac surgeons in Jaipur:

1. Expertise and Experience

Dr. Jaiswal’s years of experience in heart surgery, including performing intricate cardiac procedures, make him an expert in his field. He uses the latest surgical techniques to achieve the best outcomes for his patients.

2. Patient-Centered Care

Dr. Jaiswal believes in a personalized approach to patient care, ensuring that each patient receives the time, attention, and care they deserve throughout their treatment journey.

3. Advanced Surgical Techniques

With proficiency in Minimally Invasive Heart Surgery, Dr. Jaiswal offers a state-of-the-art approach that minimizes pain, scarring, and recovery time for his patients. His focus on precision and patient comfort sets him apart from other surgeons.

4. State-of-the-Art Facilities

Dr. Jaiswal operates in hospitals equipped with the latest medical technology, ensuring that patients have access to the most advanced treatments available. The facilities are well-equipped to handle even the most complex heart surgeries.

5. Compassionate Follow-Up Care

Heart surgery is just the beginning of a patient’s journey toward recovery. Dr. Jaiswal places a high priority on providing excellent follow-up care, ensuring his patients continue to recover smoothly and receive the guidance they need to live heart-healthy lives.

Conclusion

If you or a loved one is in need of heart surgery, Dr. Saurabh Jaiswal is one of the best cardiac surgeons in Jaipur. His experience, advanced surgical techniques, and commitment to patient care make him a top choice for heart surgeries, including Minimally Invasive Heart Surgery in Jaipur. Trust Dr. Jaiswal with your heart health, and experience the difference of world-class treatment right here in Jaipur.

To schedule a consultation or learn more about heart surgery options, contact Dr. Saurabh Jaiswal’s clinic today!

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drsumitblog · 9 months ago

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What can you do for bleeding varicose veins?

Say goodbye to the unsightly pain and discomfort of bleeding varicose veins with our advanced treatment options. From minimally invasive procedures to customized care plans, we are here to help you achieve healthier, happier legs. Contact us today for a consultation and take the first step towards smoother, happy legs.

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govindtbrc · 15 days ago

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Peripheral Micro Catheters Market: Advances in Minimally Invasive Vascular Procedures up to 2033

Market Definition

The Peripheral Micro Catheters Market includes devices used in minimally invasive procedures for the diagnosis and treatment of various medical conditions. These micro catheters are smaller in diameter than traditional catheters, allowing for enhanced precision and access to peripheral vessels, which are difficult to reach with standard-sized catheters. They are used for a variety of applications, including angiography, angioplasty, embolization, and other interventional procedures in cardiology, neurology, and oncology.

To Know More @ https://www.globalinsightservices.com/reports/peripheral-micro-catheters-market

The Peripheral Micro Catheters Market is anticipated to expand from $1.2 billion in 2023 to $2.5 billion by 2033, with a CAGR of approximately 7.5%.

Market Outlook

The Peripheral Micro Catheters Market is experiencing significant growth, driven by the increasing demand for minimally invasive procedures in healthcare. The rising prevalence of chronic diseases such as cardiovascular disorders, cancer, and neurological conditions is contributing to the growing adoption of interventional techniques, thereby boosting the demand for peripheral micro catheters. These catheters enable healthcare providers to perform delicate procedures with greater accuracy, reduced trauma to patients, and faster recovery times, which is leading to their rising popularity in the medical field.

Technological advancements in catheter design are another major factor propelling market growth. Innovations aimed at improving the flexibility, steerability, and durability of peripheral micro catheters are allowing for better procedural outcomes. Furthermore, the development of next-generation micro catheters with enhanced features, such as advanced coatings to reduce friction, antimicrobial properties, and improved radiopacity, is attracting attention from healthcare providers, contributing to the market’s expansion.

The demand for peripheral micro catheters is also being driven by the growing trend toward outpatient and ambulatory procedures. With a preference for minimally invasive options, many patients are opting for procedures that require less recovery time and hospital stay, further increasing the adoption of peripheral micro catheters. Additionally, the increasing availability of diagnostic imaging systems such as ultrasound, MRI, and CT scans is improving the accuracy and efficiency of interventional procedures, which in turn supports the demand for precision devices like peripheral micro catheters.

Request the sample copy of report @ https://www.globalinsightservices.com/request-sample/GIS32135

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himalayaneyeinstitute · 17 days ago

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The Role of Retina Hospitals in Managing Eye Emergencies

While some eye problems develop slowly, some strike suddenly. Eye emergencies need fast access to specialized care so that vision can be protected and further risk can be avoided as much as possible. Timely and expert eye care is vital to vision preservation and loss.

From trauma to the eye and retinal detachment to haemorrhages and infections, eye emergencies can happen without warning. For comprehensive eye care, you can visit the top retina hospital in Siliguri City.

Recognizing Eye Emergencies

Any abrupt or sudden trauma, injury, or acute condition that needs to be treated right once to avoid vision loss or sequelae is referred to as an eye emergency. Typical eye emergencies are:

Retinal Detachment: If left untreated, this dangerous disorder causes the retina to separate from the underlying tissue, which may cause visual loss. Vitreous Haemorrhage: Bleeding into the vitreous humour that results in abrupt changes in vision or blurring is what is known as a vitreous haemorrhage in medical terms. Eye Trauma: This is defined as injuries that may harm the retina and are brought on by forceful force, sharp objects, or chemical exposure. Blockage: Blocked blood flow in retinal vessels, also known as retinal artery or vein occlusion, causes abrupt and often severe visual loss.

Acute outcomes such as diabetic vitreous haemorrhage or tractional retinal detachment are examples of diabetic retinal emergencies. These complications can come without warning and worsen quickly, which tells how critical it is to get expert care right away.

Why Are Retina/ Eye Hospitals Essential in Managing Eye Emergencies?

The diagnosis and treatment of complicated retinal disorders and injuries are the areas of expertise for retinal or eye hospitals. Their infrastructure, service, and experience make them ideally equipped to manage all types of eye crises. Retinal hospitals are essential in the following ways:

Specialized Retinal Care

A reputed retina hospital in Siliguri has the top ophthalmologists or retina specialists trained to handle complicated eye conditions, such as eye emergencies. Their experience allows them to offer accurate diagnosis and fast treatment, which are essential in eye emergencies where delays can lead to further damage.

Advanced Diagnostic Tools

Modern diagnostic tools including Fluorescein Angiography, Optical Coherence Tomography (OCT), and sophisticated ultrasound imaging allow retinal hospitals or clinics to fast determine the severity of the eye condition. Early diagnosis helps patinets get the best possible eye care and outcome.

Emergency Surgical Facilities

Emergency surgical procedures in Siliguri like as vitrectomy and retinal reattachment surgery often performed in retinal hospitals in Siliguri. When treating diseases like retinal tears or detachment, procedures including scleral buckling, laser photocoagulation, and pneumatic retinopexy are essential.

Vitrectomy is a medical eye treatment/ procedure to remove blood, scar tissue, or vitreous gel to repair the retina. Laser therapy is used for sealing retinal tears, reducing abnormal blood vessels, or managing diabetic emergencies. Wise to choose retina eye care in Siliguri which offers surgical facilities available 24/7 to ensure timely care during emergencies.

Management of Retinal Vascular Emergencies

To minimize damage and restore blood flow, conditions like retinal artery or vein occlusions need to be treated very fast. To treat edema, bleeding, or obstructions, retinal hospitals provide procedures including intravitreal injections, which administer drugs straight to the retina. Reach out to the most trusted eye hospital at your nearest location.

Comprehensive Care for Diabetic Retinal Emergencies

Retinal problems such as macular oedema, retinal detachment, or vitreous haemorrhage are more common in diabetic patients. Modern laser treatments, anti-VEGF injections, and, if necessary, surgery are available in retinal hospitals to treat these issues or medical emergencies because of these eye problems.

Retinal hospitals or eye hospitals are essential in these situations because they provide prompt, specialized, and advanced care. Eye hospitals ensure that patients receive precise diagnoses and accurate medical care, which is most important for maintaining eye health and vision at this time. Reach out to the best retina hospital in Siliguri and meet the leading eye doctors and surgeons today.

#retina hospital in Siliguri #retina eye clinic in siliguri

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samreensway · 21 days ago

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Communication Skills Station of Call to Vascular Consultant for Acute Li...

Communication Skills Station of Call to Vascular Consultant for Acute Limb Ischemia | MRCS B OSCE - MOCK EXAM Video Description: Welcome to this MRCS B OSCE mock exam session where we focus on a crucial communication skills station: a call to a vascular consultant for acute limb ischemia. In this video, you’ll observe a structured and professional approach to managing the call in a clinical setting. Whether you're preparing for the MRCS B OSCE, clinical examinations, or improving your communication skills in medical practice, this video is an essential resource. 🎯 Video Overview: This communication skills station demonstrates how to handle the call to a vascular consultant about acute limb ischemia, a time-sensitive and life-threatening condition that requires rapid diagnosis and intervention. We will go through the important communication strategies that should be employed when discussing critical issues like ischemia with senior consultants, especially in high-pressure situations. 🚨 What is Acute Limb Ischemia (ALI)? Acute Limb Ischemia is a severe condition where there is a sudden decrease in blood flow to the limb, resulting in potential tissue damage, gangrene, or even loss of the limb if not managed quickly. The causes can vary, including embolism, thrombosis, or trauma. When presenting this case to a vascular consultant, clear, concise, and thorough communication is vital to ensure that the patient receives appropriate treatment. 🩺 Objective of This Mock Exam: In this MRCS B OSCE mock exam scenario, you’ll learn how to: Demonstrate clear and concise communication with the vascular consultant. Discuss the patient’s history, clinical presentation, and risk factors. Provide important clinical findings, including pulse loss, cold skin, and pain. Take appropriate action by escalating care quickly and discussing treatment options (such as surgery or thrombolysis). Effectively manage the clinical handover in high-pressure situations. 📌 Video Chapters: 00:00 - Introduction to Acute Limb Ischemia & MRCS B OSCE Overview Overview of acute limb ischemia: pathology, causes, and outcomes. Importance of communication skills in managing critical conditions in the MRCS B OSCE. 01:00 - Case Presentation and Patient Information A detailed presentation of the patient’s medical history and risk factors (e.g., previous vascular disease, atrial fibrillation, recent trauma). How to organize your thoughts before making a clinical call. 02:00 - Communication with Vascular Consultant Demonstrating the call to the vascular consultant: How to efficiently communicate essential details (patient demographics, clinical presentation, symptoms). Discussing clinical findings: loss of pulses, cold extremity, severe pain. Ensuring clear and concise delivery of critical information in time-sensitive situations. 03:00 - Effective Communication Tips for MRCS B OSCE How to use structured communication (e.g., SBAR format) to improve clarity and ensure nothing is missed. Importance of assertiveness and clarifying doubts with the consultant. Using professional language to instill confidence and ensure accurate handover. 05:00 - Discussion on Management Plans Vascular consultant’s response: managing acute limb ischemia with medical or surgical options (e.g., thrombolysis, bypass, or amputation). The role of escalating care when necessary. Discussing the need for immediate intervention in ischemic limbs to save the patient's life. 07:00 - Psychological Aspects of Communication Handling anxious family members and managing expectations in urgent care scenarios. Practicing empathy and active listening when speaking to the family or the patient. 08:00 - Post-Call Documentation & Follow-up Recording details of the call in the patient's medical chart. Ensure that all management steps, discussions, and agreed-upon interventions are documented. 09:00 - Final Tips for MRCS B OSCE Communication Skills Stations Key points for successfully navigating communication scenarios in MRCS exams. How to structure your responses to ensure you cover all necessary details in a calm and organized manner. Example questions that might be asked by the consultant during the call. 10:00 - Conclusion & Further Resources for MRCS B Preparation Recap of the major points discussed in the video and strategies for practicing clinical handovers. 📝 Additional Resources for MRCS B OSCE Preparation: Join Our Channel Membership to access exclusive study materials, mock exams, and more: Click here to join. Related Videos: Surgical Communication Skills in OSCE Watch Here Critical Care Scenario: Polytrauma with C-Spine Injury Watch Here Managing Medical Emergencies in OSCE Watch Here Bli medlem i kanalen för att få åtkomst till flera förmåner: / @samreenmalik #medicaleducation #education #edit #samreensway #communication #skills

#youtube #MRCSBOSCE AcuteLimbIschemia MedicalCommunicationSkills VascularSurgery OSCEPreparation MedicalExams CriticalCareCommunication SurgicalCommun

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iammikebrown6 · 22 days ago

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Pain in Legs and Left Arm: Could It Be Vascular Disease?

Pain in the legs and left arm is often alarming, particularly when these symptoms occur simultaneously. Although numerous health conditions can cause such discomfort, one potential culprit that deserves attention is vascular disease. Vascular diseases affect blood vessels and can lead to restricted blood flow, causing pain in various parts of the body, including the legs and arms. If you have pain in legs and left arm, this article delves into the possible vascular causes of pain in the legs and left arm, emphasizing the role of advanced diagnostic tools, such as Doppler systems, in identifying these conditions.

The Role of Vascular Disease in Causing Pain

Vascular disease encompasses a range of conditions that impact the blood vessels, including arteries, veins, and capillaries. When these vessels become narrowed, blocked, or otherwise damaged, the flow of oxygen-rich blood to the tissues is compromised. This can result in pain, tingling, or numbness in the affected areas. Among the vascular conditions that might explain pain in the legs and left arm are Peripheral Artery Disease (PAD) and Thoracic Outlet Syndrome (TOS).

Peripheral Artery Disease (PAD)

Peripheral Artery Disease (PAD) arises when the arteries supplying blood to the limbs become narrowed or obstructed due to plaque accumulation, a process known as atherosclerosis. PAD most commonly affects the legs, causing pain, cramping, or fatigue, especially during physical exertion. This pain, known as claudication, usually subsides with rest.

However, PAD is not limited to the legs. The disease can impact arteries throughout the body, including those supplying the arms. When plaque buildup occurs in the arteries leading to the left arm, it may cause symptoms similar to those experienced in the legs, such as pain, weakness, or numbness.

Risk factors for PAD include smoking, diabetes, hypertension, and high cholesterol. If left untreated, PAD can lead to severe complications, including non-healing ulcers and an increased risk of heart attack or stroke.

Thoracic Outlet Syndrome (TOS)

Thoracic Outlet Syndrome (TOS) is another vascular condition that can cause pain in the left arm. TOS occurs when blood vessels or nerves in the space between the collarbone and first rib (the thoracic outlet) become compressed. This compression can impede blood flow to the arm, leading to pain, tingling, and numbness. In extreme cases, reduced blood flow may result in swelling and discoloration of the arm.

TOS can develop due to physical trauma, repetitive movements, or anatomical variations. Vascular TOS specifically involves the compression of veins or arteries, which can cause considerable discomfort and may necessitate surgical intervention to alleviate the compression.

The Importance of Accurate Diagnosis

Accurately diagnosing vascular conditions is crucial for effective treatment and for preventing long-term complications. Symptoms of vascular disease, such as pain in the legs and left arm, can easily be mistaken for other musculoskeletal or neurological issues. Therefore, precise diagnostic tools are essential in identifying the true cause of these symptoms.

How Doppler Systems Aid in Diagnosis

Doppler systems are invaluable for healthcare providers striving to diagnose vascular conditions with precision. These advanced systems enable clinicians to assess blood flow and identify abnormalities in the arteries and veins with high accuracy. Here’s how Doppler systems contribute to diagnosing vascular diseases:

Doppler Ultrasound for Blood Flow Analysis: Doppler ultrasound is a non-invasive method that uses high-frequency sound waves to visualize blood flow through the blood vessels. By assessing the speed and direction of blood flow, clinicians can detect blockages, narrowing, or abnormal patterns indicative of conditions like PAD or TOS. Doppler systems provide clear, precise readings, allowing physicians to diagnose vascular issues early and develop appropriate treatment plans.

Ankle-Brachial Index (ABI) Measurement: The Ankle-Brachial Index (ABI) test is a common method for assessing PAD. This test compares blood pressure readings in the ankle and arm to determine how well blood is flowing to the limbs. A significant difference in pressure between these areas may indicate PAD. Doppler systems are designed to perform ABI measurements efficiently and accurately, offering crucial insights into the patient's vascular health.

Portable and Versatile Diagnostics: Doppler systems are known for their portability and versatility. These systems can be utilized in various clinical settings, from hospitals to outpatient clinics, enabling healthcare providers to conduct vascular assessments as needed. The ease of use and high-quality results provided by these systems make them essential tools in diagnosing conditions that might cause pain in the legs and left arm.

Treatment Options for Vascular Disease

Once a vascular condition is diagnosed accurately, treatment can commence. Depending on the condition's severity, treatment options may include lifestyle changes, medications, or surgical intervention. For example, patients with PAD may be advised to quit smoking, engage in regular exercise, and manage their blood pressure and cholesterol levels. In more severe cases, procedures like angioplasty or surgery may be required to restore proper blood flow.

For individuals diagnosed with TOS, physical therapy is often recommended to relieve pressure on the blood vessels. However, when vascular TOS causes significant blood flow obstruction, surgery might be necessary to remove the compression source.

Conclusion

Pain in the legs and left arm could indicate underlying vascular disease, such as Peripheral Artery Disease (PAD) or Thoracic Outlet Syndrome (TOS), both of which can impair blood flow and cause significant discomfort. Early and accurate diagnosis is vital to prevent complications and ensure effective treatment.

Advanced diagnostic tools like Doppler systems play a critical role in detecting these conditions. By providing clear insights into blood flow abnormalities, these systems assist clinicians in diagnosing and treating vascular diseases that might be causing pain in the legs and left arm.

For more information on how Doppler systems can aid in diagnosing vascular conditions, reach out to learn more about the available options.

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