Monthly Clinical Meeting

Added: 2026-05-25

[00:00:07]Who knows how quick a shiver can make you collapse? It's a matter of time when your body surrenders to this invisible killer. Sepsis doesn't wait. So, it's important that we spot it, treat it to beat it because every minute counts. Our first speaker today, Dr. MHF Hazina senior register in emergency medicine will enlighten us on compensator till collapse an approach to sepsis at the emergency department. Over to you Dr. Hassina Septic shock is the subset of sepsis with circulatory and cellular metabolic dysfunction conferring higher mortality risk. With that we'll move on to the implementation strategies that was assured in a new 2026 guidelines. They call of a word called sepsis or sepsis hurdle which is a multi-disiplinary team approach at bedside to discuss and ex uh dis discuss and expedite sepsis diagnosis and treatment following a positive sepsis screen. So this multi-disiplinary teamwork involve the emergency physician uh intensivist radiologist microbiologist as well as other clinical specialities for the source control. So we will move on to see what this positive sept sepsis screen is. So what are the tools that we have for sepsis screening? I think these terms are not unusual for you. I think you have heard these things. News 2, news, muse, s and Q. So far news 2 is the most recent addition with two parameters.

[00:05:56]Okay, with regard to the septic screening tools, the new tool is the most recent addition for the tools and it has a sensitivity of 73% and specificity of 82% and it is the best tool and because of uh it uh now it was a recent addition actually and it has two saturation parameters for obstructive lung pathologies as well. But as you can see the sus and Q sofa is outdated now Q so far 3% and it is not recommended alone and it is still useful due to clinical deteration. Now this is a very important finding in new sepsis guidelines where they say the QOA tool can be used at a clinical setting when a patient is admitted to a ward. it can be used by a nursing officer or a medical officer for the deterioration to detect the deterioration of the patient. So actually this has shown that the patient uh uh patient's mortality uh mortality uh rate has improved at 90day uh time period. So it is a positive finding for QFO tool in the new 2026 guidelines. So we come on to a very important aspect that is lactate in sepsis. For adults with possible probable and definite sepsis or septic shock measuring blood lactate is recommended as a serial evaluation not until normalization. This is very important. We are not targeting a normalized lactate rather we are going for a serial decline. So this is called a lactateg guided therapy and it has proven in mortality benefit when compared with the other gold directed therapies. So what is the decline that you are expecting more than 10% reduction every 2 hour. So as for an example if a patient has selected level of five if your v suppresses and fluid therapy is working at about 2 hours his lactate should be around 4.5. So I would like to have your um uh concern over the last statement as well. It is of intermediate lactate elevation between two to four is associated with increased mortality and this is the type of the patient that we discussed in the clinical scenario one where the patient had a cryptic shock. So early fluid resuscitation is mandatory to avoid progression to overt hyperfusion or shock.

[00:08:15]So we will move on to hemodynamics in sepsis with regard to the fluid resuscitation using balanced crystalalloid over.9 saline is recommended and it is upgraded from moderate evidence to strong evidence and for the traumatic brain injury person patients uh still.9 saline is recommended. Now there was a map target in the oldest old uh guidelines uh same map around 65 is beneficial but here in the new 2026 guidelines they prefer a permissive hypertension for the patient elderly patients more than 65 years of age. The trial is 65 trial where they had uh compared permissive hypertension versus usual care. So they they saw a similar 90-day mortality uh but less vasopressor exposure as well as reduced mortality at a longer follow-up. So this is a very positive finding with regard to permissive hypertension map target 60 to 65 for the elderly patients more than 65 years. So how can we give fluids in sepsis? It is rather a definitive quarter 30 ml per kg in first 3 hours and it it is uh directly associated with reduction in mortality as well as better resolution of hypertension. The interesting factor is that guidelines recommend even in heart failure and in endstage renal disease patients. So 30 ml per kg fluid bololises fluid resuscitation within the first 3 hours is recommended in endstage heart failure and renal disease as well. So this statement is evident by a rice trial, process trial and promise trial and uh all also for the obese patients BMI more than 30 they have asked to calculate adjusted body weight using the actual body weight for the fluid resuscitation and also to use dynamic parameters like uh stroke volume variation, pulse pressure variation and IVC collaps collapsible to dynamic variation over the static measurements like individual BP individual CVP individual IVC diameter measurements. So dynamic is always favored over static.

[00:10:25]So this is the comparison between the fluids that we can use. Uh so first is balanced crystalalloids. It is upgraded from moderate evidence and it shows reduced mortality. But someone might ask why what about the lactate levels in the balanced crystalalloid does not does it not affect the lactate level in sepsis.

[00:10:43]It's rather not because the lactate level in balanced crystallid physiological imbalanced crystallid and it is metabized in liver to make bicarbonate and that's bicarbonate and also in one lit of balanced crystal 8 mm moles of lactase which is not enough to has cause a detrimental effect in septic so 979 is widely used in sepsis as well as chromatic drainage But we have to be cautious because it can cause hypocchloric acidosis as as well as acute kidneys. Alb there is no benefit in mortality at 28 days or 90 days. But there are incidences where it has been used following large crystalloid resuscitation and also in cerosis because of hypoalamineia.

[00:11:36]But even though it has been used there is no effect of albine on prioritized patient centered outcomes. Evidence is by albio trial and safe trial starch and gelatine. There is strong recommendation against the usage.

[00:11:50]Now we will move on to the vasopress in sepsis. Evidence suggests there is no evidence uh for early versus delayed administration of se uh no no epinephrine or ionotropes in uh septic management. So this is uh this is uh proven by clover randomized clinical trial. There is no mortality difference but there is one exception which is unstable septic shock defined by severe hypotension model skin cyanosis altered mentation. So at if a patient has unstable septic shock yes you can introduce vasopresses at an early stage and peripheral vasopressors are always safe and feasible rather than going for a central catheterss.

[00:12:35]So this is the summarized version of all the things that was uh stated in the uh 2026 NIP guidelines. So first line is no epipine over dopamine, epinephrine, celipresin and vopricin and the rate of 0.05 to2 mics per kg per minute. Voprein is the second line. Actually the meta analysis say reduction in mortality against no epinephrine monotherapy and when it is used as an achant actually it use it reduces the tachiaria possibility as well mainly the atrial fibrillation and where we where do we start this vasopressin is when the no epinephrine do has been escalated more than.3 mics per kg per minute that is where uh you can start on the voing the dose is 01 to 04 units per minute adrenaline is the third line and whenever the vasopressin is not available you can go as the second line at a dose of 01 to 2 mics per kg per minute and dobutamine when there is persistent hypertension and there is cardiac dysfunction with rel related to the septic shock and uh there is no evidence with regard to mil neuron uh there is only insufficient evidence and the dose is 2 to 20 mics per kg per minute and there are two special things in the new guidelines about the anotensin 2 and methyline blue anotin In two uh with regard to that meta analysis suggest it may result in a reduction in mortality but it is low certainty evidence. The drawback here is it has uncertain effect of ventricular arhythmias is eskemia and deep vent thrombosis. So the dose is 20 to 200 nanog per kg per minute and methyline blue it may improve blood pressure and uh but there is only insufficient evidence to use as rescue therapy to improve survival actually 25% of clinicians favored positively to use it in a wayic shock as for my personal experience I have given methylene blow in a septic shock where we actually intubated the patient uh following the management but successfully uh exubated ated the patient on the third day because the patient improved with the methyline blue administration. So yes, it is clinician's preferred.

[00:14:48]So we will go for antibiotics in sepsis.

[00:14:51]So actually it does not uh there are no major changes in new guidelines and uh when the sepsis is definite or probable whether it whether it is associated with shock or uh not we usually go for antibiotic within 1 hour duration. When the sepsis is possible with shock, we go for antibiotics within 1 hour duration.

[00:15:14]And if the sepsis is possible without shock, uh there is a time period of 3-hour duration. So early administration of appropriate antimicrobial is the most effective initial intervention along with fluid resuscitation. So what's new in antibiotic management in new sepsis guideline? Uh so prehosp antibiotics may reduce 28 day mortality. Now we have very successful patient recruitment uh system critically ill patient recruitment system that is 1990 ambulance service. So if the paramedics were uh taught about this sepsis screening tool we could have implemented about the recognition of this patient deterioration whether it is attributed by septic shock or sepsis. So what they say is if the transportation exceeds more than 60 minutes yes we can give IV antibiotics on the transportation itself and also uh we tend to give anorobic coverage unnecessarily at our clinical settings. Majority of septic patients are of lung or urinary origin and new evidence that they are unlikely to benefit from empiric coverage necrotising soft tissue infections head and neck infection gynecological obstetric and abdominal infection and deepseated absess. Other than this there is no indication for empirical anorobic coverage.

[00:16:41]So uh there are another important factors about prolong infusionation. This is a strong recommendation. The pathophysiology behind is to keep the therapeutic level more than minimum in inhibitory concentration of the plasma and they recommend deescalation of antimicrobial therapy once the micro microbiological diagnosis is available and also they favor in shorter or longer duration of antimicrobial therapy. So these are new things in the uh 2026 guidelines. So now we are going for the last few slides. uh first adjunctive and additional therapies in sepsis. So IV corticosterois had been used in sepsis patients but in nas guidelines they recommend only in septic shock and they have done a meta analysis which which actually shows that there is shock reversal at 7 days and of course they have uh they have thought about the preferred regime as well. They have compared uh the intermittent dosing of hydrocortisone over 24 hours with a daily doses that is adrenal trial and they have found there is no mortality benefit between the two. So either we can go for uh an intermittent dosing or we can go for single daily dose. So the maximum benefit plateau is achieved at 260 mg per day and antibiotics, IV vitamin C, IV immunoglobiline, probiotics, beta blockers and vitamin D do not have mortality benefit and recommendation is against using them.

[00:18:19]Uh so this is the executive summary I want to give and this uh gives all of the new recommendation upgraded version versions of the new sepsis guideline uh 2026. The upgraded ones are prolonged betalactam infusions uh suggested by link three trial corticeroids in septic shock and clinical evaluation for diagnosis and monitoring of sepsis rather than using proalacetonine and new recommendations are code sepsis and sepsis hurdle protocol prehosp sepsis screening prehosp antibiotics within 1 hour and map 60 to 65 in elderly patient more than 65 and also due to time restriction I have not included the respiratory support in sepsis in this uh presentation but they suggest using hyponal canula over any conventional oxygen therapy and uh non-invasive ventilation in acute hypoxmia in sepsis and also active fluid removal is suggested and insufficient evidence is there for time limited trials oral midorine and milon and also for methyline thank you very much for your patient listening I think u uh this is not sufficient time to discuss about sepsis. Anyway, I think you got anything something with regard to my presentation. Thank you very much for listening.

[00:19:42]>> Um, thank you Hina for a clear and concise presentation. It's well done. So I have one uh question. Uh, what is the place of proalcitetonine in sepsis and septic shock? Uh so proalcitetonine is a nonspecific biioarker. It act actually uh in old times it was used to uh screen sepsis as well as diagnose and also for antibiotic stewardship. But now they have found out it is not only sepsis that increase the procetonine level but also stress conditions postsurgery and also other multiorgan dysfunction can improve the procetonine level. So therefore for sepsis screening and diagnosis there is no place except for one place where we can actually decide on the duration of time of the therapy that is antibiotic storage.

[00:20:35]>> Thank you. The one more question uh in new guidelines so in sepsis 2026 they mention about active fluid removal after resuscitation. What is that mean and how you going to do it?

[00:20:49]>> Yes sir. Uh so even in any physiologic patient they are they are recommending 30 ml per kg fluid kota within the first 3 hours and after that depending on the patient physiology we can go for liberative or restrictive fluid strategies. Once patient is out of the resuscitation phase they have found out removing the fluid actively actually has a better mortality benefit and survival rate. Therefore they recommending renal replacement therapy as well as IV diuretics and depending on patient's physiology whether he's in a heart failure or in stage renal failure we can escalate it up uh with a less time duration.

[00:21:27]>> Okay. Thank you very much.

[00:21:38]>> Thank you Dr. Hina for that eye openening presentation and interesting question and answer session. Moving on.

[00:21:46]It becomes a time of diagnostic chaos when you don't know what's going on nor when your patient can't explain what he or she is feeling. Just a behavioral change, an extra hour of sleeping or just refusing to eat, drink or play.

[00:22:02]Dr. Peru Pereira, senior registister in emergency medicine will guide us through these unheard voices. Pediatric shock open in the right path at the right time. A systematic line of identifying what's going on. Over to you, Dr. Pendrew.

[00:22:34]Good afternoon and thank you for setting such a great foundation for what we are about to cover now. So let's move to the other end of the spectrum the neonates and let's see how we open the right path at the right time.

[00:22:49]So we will be going through a clinical case first.

[00:22:54]How to approach to a sick infant in the ED, cardiogenic shock, newborn circulation and the management to a neonate with shock.

[00:23:09]So let me take you through the case. So, we had a 7-day old baby girl with an unremarkable postnatal cause presenting with 6 hours of poor feeding and irritability.

[00:23:22]And we also found that the baby had no wet diapers for 6 hours and with a positive contact history, the mother with febrial illness and uh the other systemic review was unremarkable.

[00:23:37]She was born at 37 weeks by emergency lower segment cesarian section and was uncomplicated had an uncomplicated perinatal history and she was the first child of non-consanguinous parents.

[00:23:53]>> So in the primary survey she she had a good cry there were no recessions respirator rate was 60 clear lungs. The saturation in bilateral upper limbs were recorded as 98% with oxygen. Lower limbs were not recordable.

[00:24:10]She had cold peripheries, mortal skin, prolonged capillary fields at 5 seconds.

[00:24:16]Blood pressure was pulse was 154 per minute low volume and the peripheral pulses. The brachia was weak. Bilateral femorals were even weaker.

[00:24:27]However, we did not hear any murmurs.

[00:24:29]The blood pressure was unable to record despite appropriate cough.

[00:24:36]She had a CBS of >> 55 temperature 36.1 hepotogali of 5 cm ectaric and the anterior fontel depressed depressed. So history and primary survey are consistent with shock as all of you can see in this neonet with differential considerations of septic shock in the context of contact history and hypothermia.

[00:25:04]Cardiogenic shock given hypotogaly and differential saturations hypoalmic shock suggested by low urine output and poor feeding.

[00:25:15]Next we have our bedside investigations.

[00:25:17]The arterial blood gas which revealed a severe metabolic acidtosis with a pH of 6.9, hyponetriia, hypercalemia and race lactates.

[00:25:31]And this is the chest X-ray showing some pulmonary congestion.

[00:25:36]We also did an ECG to look for any arhythmias leading to shock.

[00:25:43]When we had a look with the ultrasound scan, we noted that he had a good contracting heart with abnormal chamber appearance. IBC was full. No fluids were noted elsewhere.

[00:25:57]Um so narrowing down from the history examination and the initial investigations, think about what could be going on here and differentials we came across were neonatal sepsis with shock as there was a contact history and hypothermia.

[00:27:28]So moving on uh narrow down different as well were neonatal sepsis with shock as the neonate had contact history and hypothermia duct dependent congenital heart disease as the age at presentation coincided perfectly with the ductal closure at around 7 days and there was differential satur saturations, absence of recessions, weaker femoral pulses and hepotogalene and then comes congenital adnal hypoplasia as a child with hypoglycemic hyponetriic and hypercalemic with acidosis and shock and then the inborn errors of metabolism acidosis hypotogali ectaras hypoglycemia with clear lungs all pointing towards that and then comes the persistent pulmonary hypertension of the newborn as the child was in respiratory distress and differential saturations.

[00:28:25]So with this differentials in our mind, our initial stabilization started with high flow oxygen. Oxygen should never be withheld in a critically ill child even if you're suspecting a duct dependent leation and we gained IV access. We took bloods for septic and metabolic screen and we started IV dextrose for hypoglycemia and careful fluid resuscitation with 5 ml per kg alicots as we were suspecting a cardiac lesion and the critical step to this management was starting proaglandine since we were since we had a high suspicion for this to be a duct dependent leion and we covered the neonate with IV broadspect antibiotics as that is the most common neonatal emergency presented to the emergency department. Warm the patient and finally with our resuscitation the child improved clinically and biochemically.

[00:29:29]So the baby was rushed to the echo cardiogram and was found to have a severe jaxtooductal coctation of aorta, small oas, restrictive PDA, large VSD, small LV and severe pulmonary hypertension and she was transferred to catlab for balon dilotation of coctation of iota.

[00:29:53]So let's see what to do if this child comes to you.

[00:29:58]Neonatal emergencies are a diverse group of conditions and in the emergency department we rely a lot on pneumonics not because we love them but it helps to reduce the cognitive load and it helps to support rapid and accurate clinical decisions in the emergency department.

[00:30:18]So this is one such pneumonic the misfits.

[00:30:21]So trauma, heart disease, endocrine, metabolic, inborn errors of metabolism, seizures, formula problems, intestinal disasters, toxins and sepsis are the diagnosis that are critical that you need to think about.

[00:30:40]So just going through the basics, you're going to know this. Babies are not small adults. So there are lots of physiological differences between adults and babies. Uh shocking children therefore behaves differently in children. So here what we see is the cardiac output is heart rate dependent and the stroke volume is relatively fixed in children. Therefore tachicardia means primary compensation to shock and initially there is a period of tachicardia without conccommittent drop of blood pressure. And as the shock progresses, the child deteriorates rapidly into decompensation.

[00:31:24]>> And we're talking about cardiogenic shock here. So which which is defined as pump the causes could be primary due to cardiac diseases itself or it could be secondary due to sepsis drug induced causes other than cardiac.

[00:31:43]So how do you differentiate cardiogenic shock from other types of shock? So of course you need history, examination and investigations. In history the witch has pain, syncopy, palpitations, preceding viral illnesses, pre-existing cardiac disease, examination enlarged liver, gallop rhythm, murmurs, rails, distended neck vessels, weak peripheral pulses, arrhythmias, abdominal distension, edema and crackles.

[00:32:12]and chest X-ray will reveal enlarged heart and pulmonary venus congestion.

[00:32:19]Also, if the child is deteriorating due to fluid bolus administrations, you can think of this.

[00:32:37]So in order to identify slam so let me brief you on this um and there are some defects the baby's heart is structurally unable to maintain the circulation without this fetal shunts. So here you see the oxygenated blood from mother enters the right side of the heart.

[00:33:00]But in your in in the fetus due to the high pulmonary vascular resistance only a small portion of blood goes to the lung and the majority of the blood will join the systemic circulation via the ductus arteriosis.

[00:33:17]And after birth as the ductus closes but in then the ductus becomes the critical lifeline to maintain the circulation which means it acts as a bypass channel directing blood to either pulmonary or systemic circulation depending on which side is obstructed.

[00:33:37]And if the duck closes the child collapses and this is where maintaining this pathway at the right time is essential for survival.

[00:33:49]So there are two types of duct dependent circulations. One is duct dependent leftsided circulation which means blood can't get to the body. So the child will come in shock as the cardiac output is low. And the other type is the right side lesions where the blood can't get to lungs. So they present with sinosis predominant picture with hypoxia.

[00:34:11]So there are five classic cyanotic congenital heart diseases uh trunkus arteriosis transposition tricuspid atreesia tetrology of fellow and tapr.

[00:34:23]So all of them no matter what leion they present to the ED when the duck closes.

[00:34:31]So about coctation, coctation can be classified into three types. In infants is mostly preductal. So closure of duct causes collapse and in older children the coctation the duct has already closed. So it's not it's not duct dependent and the body has developed collateral circulation already.

[00:34:53]So how do you go about diagnosing this?

[00:34:57]Well, you only need to classify the type of the defect. You don't need to know the specific defect. You can leave the detail anatomy hunting for the cardiologist.

[00:35:08]So, time to step into the approach to management. What are the special considerations in airway and breathing?

[00:35:16]We need to measure pre and post-ductal saturation targeting predal more than 75%. You don't need to have a saturation up to 100. You don't want to uh lower the pulmonary vascular resistance lower further and increase pulmonary flow which will compromise systemic circulation further and differential saturation is important duct dependent lesions and reverse differential saturation can be seen in TGA and unless they are in severe heart failure you may be able to hear crackles hyper peroxia test is important. It can help you to differentiate between a pulmonary and a systemic and a cardiac cause. Uh if the PO2 or the saturation rise rise with the oxygen that you are providing then you are looking at a pulmonary cause and importantly you should not withhold oxygen while awaiting diagnosis. Oxygen as we discussed is a pulmonary vessilator. So it can worsen duct dependent systemic leations and you really really there are no concerns about oxygen accelerating duct closure if you are going to start proaglandins and of course you can always stop or reduce oxygen if the hemodynamics worsen and positive pressure ventilation is also important but it can reduce preload it there is a risk of collapse in preload dependent lesions be prepared for deterioration. So ketamine epinephrine to bedside.

[00:36:55]Um if I ask you do you need a ABG or a VBG for this patient? So research continues to support VBG as a generally reliable alternative to ABG in children particularly in the ED as there is a good Venus arterial agreement for PH and bicarbonate but the carbon dioxide agreement only within the normal range.

[00:37:19]So combined with pulse oxymetry, VVG could possibly replace AVG for some patients with respiratory distress.

[00:37:29]What about high flow versus NIV?

[00:37:32]>> NIV high flow versus NIV. uh a 2026 systemic systematic review found that starting high flow and escalating to NIV when clinically indicated may be the optimal approach for most children.

[00:37:50]Of course, both have their pros and cons. High flow is better tolerated, fewer complications and NIV is superior in preventing intubation but at the cost of a lot of complications.

[00:38:06]Regarding the circulation management, always measure for extremity blood pressures. 5 ml per kg also are safer and a variety of inotropes are available for hemodynamic support. Uh out of which epinephrine is the first line. You have to titrate all these inotropes to preductile blood pressures. If it's a leftsided lesion, then doamine is preferred. Right-sided melarinon is preferred and if the child in shock you should always start epinephrine and if the child is duct dependent proaglandine infusion is your go-to option.

[00:38:43]So what about the role of proaglandines?

[00:38:46]If there is any potential for your neonate to be duct dependent start proaglandins immediately.

[00:38:55]Even if you're wrong, it's better to start proaglandine and be wrong than not start proaglandins. So if it can take about 15 minutes to start acting, you don't need to uh wait until definitive diagnosis by an echo cardiogram. You don't need central access uh and should be started and you can even stop it later once the detailed echo cardiogram is available. So what it does is it reopens the duct. It acts as a life-saving bridge to definitive surgery. The side effects and impact are dose dependent. So the important side effects here we see are apnea and hypotension. Always anticipate the need for intubation before initi initiation.

[00:39:40]And of course if you are transporting your child to a tertiary center it's always you need to intubate the child and start on proaglandings.

[00:39:52]Diagnosing cardiac diseases based on murmur is also unreliable interestingly and it has a low accuracy even in experienced hands and broadspectctrum antibiotics should be thought of as sepsis is the most common neonatal emergency. EMO early activation can be life- saving. Hypoglycemia hypothermia are frequent requires vigilant monitoring.

[00:40:18]What about sodium bicarbonate for metabolic acidosis?

[00:40:22]So many use it, but there's no good evidence to show its benefit in metabolic acidosis per se. And repeated studies over many years show no consistent benefits from sodium bicarbonate in pediatric or neonatal metabolic acidosis and may it may actually cause harm.

[00:40:45]Can we use rush protocol in pediatrics?

[00:40:48]Yes, there is latest evidence support the rush protocol as a rapid reliable screening ultrasound method to differentiate shock in pediatrics and literature also suggests the use of intraraanial ultrasound in infants with an open fontel and we can you can uh help to identify causes such as infection, hydroaphilus and hemorrhage.

[00:41:19]So to conclude the key messages are it's always early recognition of shock is critical in children due to their unique physiology. Early referral to appropriate specialty team always palpate femoral pulses in neonet differential saturation is a critical clue. The key to successful outcome in duct dependent leion is to realize that the patient is duct dependent. Start proaglandins.

[00:41:48]Don't rely on murmurs. Don't rely on lung crackles to exclude cardiac causes.

[00:41:53]Syinosis without respiratory distress or shock with clear lungs. Always think cardiac until proven otherwise.

[00:42:05]be vigilant of hypothermia and hypoglycemia and find and involved. These are my references. Thank you.

[00:42:25]>> Thank you Dr. Pindu for your very nice presentation. It's regarding a pediatric neonate with the shock. I have one question from you to you and actually in this slide you I saw that at one point that in blood pressure is not monitored and monitoring blood pressure in in I think is a crucial point and uh but the BP monitoring is challenging actually it's this this step like a very small kit how to overcome this issue and how to solve this problem.

[00:43:02]>> Yes, it's definitely challenging. So, um in neonates map is a reliable indicator than measuring solid blood pressure and it roughly uh equates to the gestational age in weeks and uh when we are measuring map the the map map less than 30 mm of mercury is not very reliable. If you're measuring map with a oscillometric technique. So the gold standard there is using invasive blood pressure measurements and here we can use umbilical artery catheterization which can be used in the immediate neonatal period failing which radial artery.

[00:43:54]Okay. Thank you.

[00:44:12]Thank you Dr. Pineru for that uh comprehensive presentation and yet another productive question and answer session.

[00:44:21]Moving on, let's see how we can apply everything that we learned in real life.

[00:44:25]We have both our senior registars Dr. Hassina and Dr. Pineru making way for the casebased rapid fire quiz. I would like to highlight that we will be having a poll at the end of each case scenario to which only the participants physically present here today will be able to send in your answers.

[00:44:51]All right. So let's put so let's your clinical thinking to test now. So in the ED it's all about quick thinking. Let's see how fast you can think on your feet now. Um so we've got a quick quiz coming up. Uh so think of this like an ED decision. uh and there'll be 10 questions 10 minutes total and at the end of all 10 questions we'll be having a discussion uh of all the we'll be discussing all the questions and answers and it's available to the physical participants and also the online participants. All the best.

[00:45:25]All the best. All the best.

[00:58:25]What's All right. So, how is it?

[00:59:11]Okay, second question.

[00:59:27]Well done.

[00:59:40]Answers are still being altered. Is it okay? Fantastic.

[01:00:06]Oh, great job. Yes.

[01:00:34]Wow, that's a straight guess, I guess.

[01:00:57]Okay. So, we will also be choosing a winner and the winner would be the one with the highest score um in the shortest time. So, we'll be announcing the winner shortly. So, um let's see how well all of you have performed now.

[01:01:25]Ah, your ED is emergency department. I mean another one. I was thinking 82 year old man coming with the ED.

[01:01:35]>> Okay. So the first question um so a 82year-old man presents to the emergency department and the vital is in shock and bradicardic.

[01:01:49]So I think most of you all had got the answer right. So let's go to the explanation. The answer is D. Uh so the EC ECG here showed a third degree or a complete heavy block and for bradicardia with the adverse features such as in this case the patient was in shock. Uh so the treatment of choice is atropane.

[01:02:15]Any questions about that?

[01:02:29]Okay. The question two.

[01:02:32]>> So this is a 72 year old man uh with some co-orbidities, diabetes, hypertension and eskeemic heart disease presenting with shortness of breath. Um were you all were able to recognize these ultrasound images?

[01:02:51]So here in the right upper quadrant there's some plural eusion and IVC is full bilateral B profile in the lungs and paresternal short axis systolic and the diastolic doesn't show much of a difference isn't it so the right answer is start for this cardiogenic shock with pulmonary edema and high filling pressures.

[01:03:19]So the correct answer is D.

[01:03:21]Uh so the initial goal in patients with cardiogenic shock and associated hypotension uh should be focus on the restoration of perusion to vital organs uh for so therefore the correct answer is no epinephrine. You can add on the other following restoration of perfusion and immediate diuretic therapy will help with pulmonary congestion. Yes. But in hypotensive shock it can worsen the perfusion further and crystalloids will definitely worsen the respiratory failure and IABP is an option but it's definitely not the first line that is after medical optimization.

[01:04:06]So question number three, 22 year old man presents to the emergency department after being ejected from a vehicle highspeed mechanism. uh uh sustained blunt trauma to chest and abdomen.

[01:04:21]He's again in shock. So what type of a shock is this? Heart rate is 141 and the paramedics have given crystalalloids.

[01:04:32]EAST is negative.

[01:04:34]>> Negative.

[01:04:35]>> So after one liter what is the most appropriate choice? So EAS being negative can you exclude hemorrhagic shock? No, you can't. So, you need to activate massive transfusion protocol targeting a lower normal systolic blood pressure and so for the diagnosis of hemorrhagic shock following highend high energy blunt trauma. So repeating e first and a CT this patient is unstable you cannot send this patient to CT and no epinephrine it will further worsen the hyperparusion Andrew emilization is an option but it's used in stable or transient responders and urgent lepertomy if the source of source of bleeding is identified. Yes. But here the EAS is negative. So there's no role of urgent laparotomy for this patient.

[01:06:12]So moving on to question number four. A 34 year old woman presents to the emergency department with breast breathlessness. She underwent an emergency laparottomy uh for perforated appendicitis 5 days ago. Uh discharge on oral antibiotics and now coming with shock. So low blood pressure, tachicardia.

[01:06:35]Um but she complains of abdominal pain but the abdomen is soft and the surgical wound is dry and no obvious external bleeding. So the mostate management is for so the first line and the life-saving intervention is IM epinephrine to the lateral thigh and you need to place the patient in supine position.

[01:07:02]Uh so oxygen, IV, steroids and histamine are appropriate adjuns but you can not use it as firstline agent and uh subcutaneous epinephrine is an incorrect option for anaphylactic shock and there is no evidence of intraabdominal catastrophe. So it does not uh explain the V and acute shock. So septic shock also a differential postoperatively but the presence of bees and acute onset breathlessness following antibiotics points your diagnosis towards anaphylactic shock.

[01:07:42]So question number five, a 30-year-old female presents to the emergency department after falling from a 10-ft ladder. She's conscious and complains of back pain. So lungs clear. So what's the difference here from other shock types?

[01:07:59]Here the patient is hypotensive and bradicardic.

[01:08:03]Uh so we are looking at u neurogenic shock here. So the correct answer is administer high flow oxygen immobilize with cervical immobilize the cervical spine IV atropene for bradicardia and initiate vasopressor support for suspected neurogenic shock.

[01:08:24]Uh why other options are wrong? Because uh if the patient is in sept uh although the patient is myop fibbrri septic shock presence with tachicardia not bradicardia and uh vasop presses and fluids are appropriate but here uh the option omits atropene and hypoalmic shock presence with tachicardia and cold peripheries and here patient is bradicardic with warm peripheries. And uh the last option observation alone is not appropriate at this stage.

[01:08:59]>> Thank you Po. So from question six onwards these are clinical based scenarios. Actually these are actual patients who presented to the emergency department. And uh question number six, it was a 59er female who came with a dense right-sided paralysis along with hypotension.

[01:09:19]As you had already correct correctly uh assumed that it was a Stanford type A iotech dissection. As you can see in the focus on the plaque sw the iotic root diameter is more than 4 cm and on common carrot there is a visible clearly visible dection flap and the parastonial short axis wave I put because uh I wanted you to exclude the obstructive shock due to secondary to pulmonary emolism and there is no right ventricular dilation or septal deviation here that is for the exclusion of one of the stems of the so the answer was clearly as 99% of you had correctly diagnosed it is acute Stanford type A iotic dissection involving the koted arteries and uh in this clinical presentation we actually went without doing an NCCT brain we actually went into doing a CTO and urgent cardiothoracic opinion and patient had a dissection flap extending to thoraxic iota as well as abdominal iota infraally so in a Stanford type a iotic dissection usually it is the surgical intervention as the prim primary therapeutic intervention. So the patient was uh taken into the surgery.

[01:10:31]So there are two types of classification for Stanford uh that is one is Stanford and other is debac and that is for your knowledge and always have to remember that iotic dissection can present as a obstructive shock as well as a hemorrhogic shock, neurogenic shock and also a cardiogenic shock.

[01:10:51]Question number seven.

[01:10:53]A 12 year old child with a fever for three days. Uh his full blood count shows um platelet reduced platelet count thrombocytoenia and hemocrit was 45 baseline hemot was 35 which shows a leaking face and the patient's blood pressure was 78 by 60 and there was a narrow pal pressure of 18 and there was right hyper contact tendons as well. What is your next step of management? So I think most of you had correctly diagnosed it. uh so it is IV normal saline bersus 10 cc per kg over 1 hour. So if you can see uh the shock algorithm in the uh Sri Lankan college of uh pediatricians where they have given a clear concise image the shock can be compensated or uh uncompensated uncompensated shock is identified by no palpable pulses as well as uh no recordable BP. So there only you give 20 cc free flowing bololises other than that your always therapeutic intervention should start with 10 cc per kg normal saline bololises in compensated shock and serial evaluation should be done and despite the crystallite bololises if the shock is persistent then you have to evaluate for ABCs that is acidosis and uh bleeding also hypocalcemia hyponetriia and hypoglycemia.

[01:12:15]So the correct answer is 10 cc per kg uh over 1 hour and uh there is no indication for 20 cc per kg over 1 hour in compensated shock and ultrasound to confirm patient leaking phase is actually uh the dent hemorrhagic fever is a rather clinical diagnosis. You do not want any ultrasonic ultrasonographical evidence to confirm patient in leaking phase.

[01:12:40]Question number eight. Uh 48 year old male diagnosed with severe depression presented with acute injection of drugs and he had taken anti-depressant as well as anti-hypotens. So patient is having a bradic cardia with shock. So this is the ECG. As you can clearly see the QT interval is more than 600 milliseconds.

[01:13:01]But there is one point you have to remember in toxicological courses we do not use the baset formula but we rather go for a crude measurement of the QT interval. visit formula does not apply in toxicological causes. So here uh it is a sort toxicity which increases the it is a class 3 antiarithmic and non- selective beta and it increases the QT interval therefore increases the tendency of VTs.

[01:13:28]uh so I I saw that most of you all had selected amitryptton toxicity in this patient but I would like to say the easy changes are rather different when compared to level toxicity there you have broad complex takardia due to colonial receptor blockage and because of the sodium channel blockage there is increased QRS complexes and there can be uh PR prolongation as well due to potassium channel blockage and also AVR positivity R to S ratio more than 7 are the pathogamagnetic features of amitroenic toxicity. So this is rather sort uh management is with hemodynamic support high therapy early pacing and overdrive pacing and enhanced elimination with hemodialysis. So in our patient we did the overdrive pacing with uh collaboration with the cardiology team.

[01:14:18]Question nine, it is about a 38 year old uh parity third uh 30 weeks of gestation patient came to the night shift of at the EU with hemoric shop BP was 60 by 40 and capillary refilling time was 5 seconds with motor skin and uh during the resuscitation patient went into a cardiac arrest. So the uh ALS algorithm was initiated and as I correctly saw you all had correctly identified it is the uh immediate period cesarian section that should be done and according to the new EAC guidelines there is no timeline for the perotm cerian section they advise to do it as soon as possible. So in our patient also we did a perotm cesarian section and patient survived for 7 days and because of the DIC uh that had already been set up due to hypothermia we could not survive the patient but uh we did the perotm section successfully at the question 10 it is about a 45 year old man diagnosed with acute pancreatitis secondary to gallstone disease presented with severe epigastric pain so there is hypotension with hypoxmia and the abdomen is also tender on the epigastrium. So you can see there are a lot of confluences mainly distributed in peripheries without any cardomegali. So this is a a ards classical ARDS picture and uh I saw that you had correctly took D as the answer distributive shock due to systemic inflammation with ARDS. Um why it is not cardiogenic shock is this picture is not telling with the pulmonary edema and also septic shock due to infected pancreatic necrosis is very unlikely in this acute presentation of the patient and hypoalmic should shock could be there because of the refractory vomiting but you have to do a rush protocol to identify the undifferiated shock. Obstructive shock due to pulmonary embelli is unlikely in this patient due to less risk factors.

[01:16:26]So this is the differentiation of pulmonary redeemer versus ARDS. I think these are simple things for you. So uh this is the end of the rapid fire case and cong congratulation to you all uh and thank you for your enthusiastic participation.

[01:16:49]>> Thank you Dr. Pedro and Dr. Hassina for that uh quite rapid yet productive uh session of uh case scenarios. So before we move on uh we have a request a vehicle number C A K6861.

[01:17:04]Apparently it's blocking one of the uh vehicles that need to leave urgently. So anyone uh who the owner of this car if you could remove it that would be great.

[01:17:14]Thank you.

[01:17:16]Right. Uh I'm sure we all got a holistic uh idea about sepsis by now. It was quite comprehensive uh both adult and pediatric. So now we have a few minutes to entertain any questions from the audience with regards to the topic today.

[01:18:14]any question.

[01:18:27]So for the emergency medicine registars and the senior registras for the asina correctly mentioned about the balance crystalide solution in sepsis management I think it need to be practiced because we all usually doing is the 0.9 saline as a usual practice but it need to be uh as balanced crystal the heart man or the eagles like uh there's a bit uh issue about the lactate in both cris and the regus lactate but uh it does not count into your actual lactate level in the patient because it produced because of the anorobic metabolism but we are given uh the additional lactate but which is going to be metabolized in the liver in the heptoite and then it produce ultimately the bicarbonate which is useful in the patient who is having acidosis in the sepsis. So make sure you use balanced crystal rather than 0.97 which might cause um the acidosis hypoglymic acidosis. So it is better to have something more closer to your plasma osmalerity and electrolyte wise and it has added advantage of neutralizing or buffering uh the patient acidosis.

[01:20:01]So make sure you shift it from 0.9 saline to uh balance crystal where you have available >> we do. Yeah, >> also just few word about the I think I did the same >> because it's a metal blue is a lifesaver. It's a refractory void. Yeah, you know what the underlying mechanism in the septic shock is once the endothelial activation get the nitrous oxide exist and it usually repracted to the vasopresses and if the requirement is go beyond three like everything and there's a place but it's independ but it's still the case report there's no wide lack of evidence but it seemed to be weak use serve and survive the patient and hope some some case studies say that the Asian population is compared with the European studies the methium blue response is good I think so that might be the thing further research regarding methyl blue and use of methyl blue inis in Sri Lankan population think but it's not available right not available but it's not available I saw sometimes you know trauma and all that too early but one of those I didn't see So in yeah in emergency department we usually I mean like we think about but we usually not do the albin level particularly because Yeah.

[01:22:07]>> 10 days >> it comes.

[01:22:14]>> Yeah. Exactly.

[01:22:16]>> Yeah.

[01:22:21]>> Right. Thank you to our expert panel for elaborating on some of the pointers.

[01:22:27]So um I would like to remind our audience about the CPD points that can be obtained from attending this session and you can uh earn 1.5 points. However, I would like to emphasize that it would be awarded to the participants physically present here today. So you can scan the QR code and uh obtain those points.

[01:22:47]So now it's time uh to extend acknowledgements to our speakers and the panelists the main efforts behind today's session. So uh I would like to call upon Dr. Kawos Latilasi the secretary of the Sri Lanka College of Emergency Physicians to present the tokens of appreciation to our speakers Dr. MHF Hassina and Dr. Pendra Pereira.

[01:25:35]Ruanti Jay, assistant secretary of the Sri Lanka Medical Association to declare the vote of thanks.

[01:25:52]Good afternoon. Um and um I would like to uh say a special thank you to Sri Lanka College of Emergency Physicians um for collaborating with the Sri Lanka Medical Association for our monthly uh clinical meeting. I think that was was a very fruitful session even though I missed the first half. Um we have about uh more than 100 online participants and um we have about 60 plus on-site participants. Um so I first of all I would like to thank uh Dr. Inuk Vijay Vijay Gunawadana president of the Sri Lanka College of Emergency Physicians for collaborating with us and organizing today's CME. Um let me thank the speakers Dr. MHF Hassina senior registister in emergency medicine. Um Dr. Dr. Pinu Pereira senior registister in emergency medicine and as well as for for the talks as well as for the uh quiz and the expert panelists again Dr. Vijay Inukawad and Dr. Bandaya let me thank office staff as well as our demonstrator Dr. Kunara for helping with the organizing of the CNB. Uh thank you very much for your participation and your active engagement. Um I would like to thank the on-site as well as the online participants. I hope you would join again with us in our next CME and we have a line of work pre-ongress workshops planned. Keep your um keep your eyes and ears open for them and I would like to um invite you for the uh main SLMA congress which is happening in July um in the 20s. Um also we have kept some registration forms to get your full membership for the SLMA. Um there are multiple benefits um and it's a nominal amount. You can get your life membership and on your way out I would like to invite you to get your SLMA membership as well. Right. Thank you.