REBEL Cast

Salim R. Rezaie, MD

Rational Evidence-Based Evaluation of Literature

  1. 15/11/2023

    REBEL Core Cast 112.0 – Awareness During Paralysis

    Take Home Points: Dose your RSI meds correctly.  Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic.   Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor!  REBEL Core Cast 112.0 – Awareness During Paralysis Click here for Direct Download of the Podcast Awareness during paralysis is real. However, data is limited in ED patients. The ED AWARENESS study found a 2.6% rate of prevalence: meaning about  three in every one hundred people may experience awareness during paralysis.  We know that rocuronium has a longer half life than its counterpart succinylcholine. However, this is not the problem! The key is starting post-intubation sedation ASAP.  We need to keep this phenomenon in the back of our minds every time we intubate. Here are some things we can do to prevent awareness during paralysis:  Dose your RSI meds correctly.  Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic.   Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor!  References Pappal, Ryan D., et al. “The ED-AWARENESS study: A prospective, observational cohort study of awareness with paralysis in mechanically ventilated patients admitted from the emergency department.” Annals of emergency medicine 77.5 (2021): 532-544. Links Staten Island EM: Only in Staten Podcast Post Created By: Anand Swaminathan MD, MPH Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 112.0 – Awareness During Paralysis appeared first on REBEL EM - Emergency Medicine Blog.

    18 min
  2. 13/12/2023

    REBEL Core Cast 114.0 – Carbon Monoxide Toxicity

    Take Home Points: Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. The symptoms of mild, acute exposure are non-specific and can be confused with a variety of other disease processes including common viral syndromes. Testing is done via co-oximetry which determines the amount of carboxyhemoglobin in the blood. Treatment is guided by supplemental oxygen which decreases the half-life of carboxyhemoglobin. Hyperbaric oxygenation should be considered in patients with severe toxicity (syncope, altered mental status, myocardial ischemia, or neurological abnormalities). REBEL Core Cast 114.0 – Carbon Monoxide Toxicity Click here for Direct Download of the Podcast Definition and Physiology Carbon monoxide is absorbed via inhalation from the incomplete combustion of any carbon containing substance. Most often, exposures often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. Toxicity is mediated through multiple mechanisms. Physiologic oxygen carrying capacity is reduced as carbon monoxide binds hemoglobin with a greater affinity than oxygen. Moreover, carbon monoxide shifts the oxygen-hemoglobin dissociation curve to the left which reduces oxygen delivery to tissues. Lastly, carbon monoxide effects cellular oxygen use by impairing oxidative phosphorylation by binding to mitochondrial cytochromes. (Goldbaum 1976) Clinical Manifestations Acute, mild toxicity presents non-specifically. Given that most exposures will occur during the winter months, a common misdiagnosis is influenza or the “common cold.” Symptoms include: headache, dizziness, nausea, vomiting, and generalized weakness. More severe toxicity will present with syncope, altered mental status, neurologic disturbance (ie. ataxia), myocardial ischemia, or cardiac arrest. Carbon monoxide poisoning may lead to delayed neurologic sequalae – a constellation of dementia, psychosis, parkinsonism, amnestic syndromes, among other neurologic impairments. Management Carbon monoxide testing is performed via co-oximetry which determines the amount of carboxyhemoglobin present. The mainstay of treatment is supplemental oxygenation. The half-life of carboxyhemoglobin drops from 5 hours on room air to 1 hour when breathing 100% oxygen at normal atmospheric pressure (via non-rebreather). Hyperbaric treatment should be considered for severe toxicity. (Goldfrank’s Toxicology 2019) Carboxyhemoglobin levels > 25% or >15% in pregnant patients are indications for hyperbarics, independent of signs/symptoms There is evidence that hyperbaric oxygenation reduces the risk of cognitive sequelae after acute carbon monoxide poisoning. (Weaver 2002) As always, call your local toxicologist or regional poison control center to help determine the need for hyperbaric therapy.   Take Home Points: Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. The symptoms of mild, acute exposure are non-specific and can be confused with a variety of other disease processes including common viral syndromes. Testing is done via co-oximetry which determines the amount of carboxyhemoglobin in the blood. Treatment is guided by supplemental oxygen which decreases the half-life of carboxyhemoglobin. Hyperbaric oxygenation should be considered in patients with severe toxicity (syncope, altered mental status, myocardial ischemia, or neurological abnormalities). References Goldbaum LR, Orellano T, Dergal E. Mechanism of the toxic action of carbon monoxide. Ann Clin Lab Sci. 1976 Jul-Aug;6(4):372-6. PMID: 962299. Tomaszewski C. Chapter 122. Carbon Monoxide. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, , Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 11e New York, NY: McGraw-Hill; 2019. Accessed November 6, 2023. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1057-67. doi: 10.1056/NEJMoa013121. PMID: 12362006. Post Created By: Sanjay Mohan MD Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 114.0 – Carbon Monoxide Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

    12 min
  3. 24/01/2024

    REBEL Core Cast 116.0 – Achilles Tendon Rupture

    Take Home Points Achilles tendon rupture is a clinical diagnosis. The Thompson Test should be applied in all suspected cases. Remember to brace or splint a rupture, even if suspected, in the resting equinus position for optimal healing and prevention of further injury. Schedule follow up with orthopedics within 1 week for discussion of operative management vs early rehab protocols. REBEL Core Cast 116.0 – Achilles Tendon Rupture Click here for Direct Download of the Podcast Achilles Tendon Rupture Exam (www.lfaclinic.co.uk) Physical Exam May have palpable gap or deformity in region of tendon. Weakness with plantar flexion. Increased resting ankle dorsiflexion on affected side in prone position with knees bent . Usually in absence of bony tenderness unless accompanied by other injury Thompson Test (video) Place the patient in the prone position, with feet hanging over the end of a stretcher or table. If patient is not able to lay down/there are no stretchers, the patient can kneel on a stool or chair Squeeze the calf of the normal limb. You will notice the squeeze will cause the ankle to plantarflex appropriately Squeeze the calf of the limb with the suspected Achilles tendon rupture.  You will notice the squeeze will cause no motion if there is a full rupture/tear, and diminished motion if there is a partial tear Performance Characteristics (Garras 2012) Sensitivity Specificity (+) LR (-) LR 96-100% 93-100% 13.7 0.04 Imaging X-Rays Used to rule out other or concurrent pathology May show soft tissue swelling and destruction of pre-Achilles fat pad (Kager’s Fat Pad) Findings are non-specific as tear of tendon unable to be visualized Ultrasound Ultrasound is helpful if obvious findings present and to distinguish between partial vs complete tears, however only around 50% sensitive for detecting only partial tears (Kayser 2005) MRI Gold-standard imaging modality Rarely, if ever, necessary in the ED Used for equivocal physical exam/alternate imaging findings or for assessing the severity of the tear for possible operative management Findings A full-thickness tear often shows a tendinous gap filled with edema or blood Complete rupture shows retraction of tendon ends ED Management Provide analgesia Tendon stabilization in an optimal healing position Functional bracing/splinting in resting equinus/talipus equinus AO splint/brace in 20 degrees of plantar flexion for 4-6 weeks (may use tall CAM boot with 20 degrees wedge inserts) All patients should be non-weightbearing Any weight-bearing can convert a partial tear to a complete tear Maintain non-weightbearing status until see orthopedics (within 1 week) After evaluation by orthopedics, early weight-bearing and early ROM exercises yield better outcomes (can be as early as 2 weeks) Referral to rehab warranted to improve plantar flexion and decrease risk of re-rupture ED Ortho consultation: patients with open wounds in the area of trauma, or with concomitant fractures Operative Management is usually reserved for acute ruptures (approximately 6 weeks) of full thickness with large tendon gaps, failed conservative treatment of partial thickness tears, or high performance athletes These cases will be determined during follow up with orthopedics and may warrant outpatient MRI to assess severity of tear Prognosis For conservative management, there is no significant difference in plantar flexion strength (Willits, 2010) Some increased risk of re-rupture compared to operative management, although review of evidence shows that this may not be significant if patients used structured, accelerated rehab protocol. Protocol includes initially non-weightbearing cast with the foot in equinus position as described above, then transitioned to a pneumatic walker with elevated heels (elevation gradually reduced biweekly), and physical therapy to improve gait, strength, and mobility. (Wallace 2011) If addressed early and appropriately, most patients have good self-reported long-term outcomes regardless of the treatment modality Links Orthobullets: Achilles Tendon Rupture Resources: Sheth U et al. The epidemiology and trends in management of acute Achilles tendon ruptures in Ontario, Canada: a population-based study of 27,607 patients. Bone Joint J. 2017; 99-B(1): 78-86. PMID: 28053261 Chiodo CP, Wilson MG. Current Concepts Review: Acute Ruptures of the Achilles Tendon. Foot Ankle Int 2006; 27(4): 305-13. PMID: 16624224 Leppilahti J, Orava S. Total Achilles tendon rupture. A review. Sports Med. 1998; 25(2): 79-100. PMID: 9519398  Kayser R et al. Partial rupture of the proximal Achilles tendon: a differential diagnostic problem in ultrasound imaging. Br J Sports Med. 2005; 39(11): 838-42. PMID: 16244194 Margetic P et al. Comparison of ultrasonographic and intraoperative findings in Achilles tendon rupture. Coll Antropol. 2007; 31:279-284. PMID: 17598414 Garras DN et al.  MRI is Unnecessary for Diagnosing Acute Achilles Tendon Ruptures: Clinical Diagnostic Criteria. Clin Orthop Relat Res 2012; 470(8): 2268-2273. PMID: 22538958 Willits K et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial using accelerated functional rehabilitation .J Bone Joint Surg Am. 2010; 92(17): 2767-75. PMID: 21037028 Wallace RG et al. The non-operative functional management of patients with a rupture of the tendo Achillis leads to low rates of re-rupture. J Bone Joint Surg Br 2011; 93(10):1362-6. PMID: 21969435 Erickson BJ. Is Operative Treatment of Achilles Tendon Ruptures Superior to Nonoperative Treatment? Orthop J Sports Med. 2015; 3(4): PMID: 26665055 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 116.0 – Achilles Tendon Rupture appeared first on REBEL EM - Emergency Medicine Blog.

    6 min
  4. 29/01/2024

    REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE?

    Background: Massive pulmonary embolism  defined as sustained hypotension (SBP 40mmHg RV enlargement defined as RV/LV ratio >0.9 Tricuspid Annular Plane Systolic Excursion (TAPSE) also recorded Tissue Doppler Derived Tricuspid Annular Systolic Velocity recorded Tei-Myocardial Performance Index (MPI/Tei) recorded CT All patients underwent 64 slice CTPA for definitive diagnosis of PE at admission Additional CTPA 24 hours after completion of thrombolysis if eGFR >60mL/min/1.73m2 Criteria for Thrombolytic Success Included: Doppler documentation of resolution of increased PASP (16mm) Systolic Wave Prime (S’) >10.0cm/s Tissue Doppler Derived RV MPI > 0.55 Clinical improvement of symptoms and restoration of stable hemodynamic status immediately after thrombolysis Complete success = Clinical improvement of symptoms and restoration of a stable hemodynamic status along with at least 3 other criteria without resultant death and nonfatal major complications Outcomes: Primary: In-hospital mortality Major complications Ischemic stroke, ICH, embolism (coronary or peripheral), bleeding requiring transfusion Pulmonary HTN while in hospital RV dysfunction while in hospital Secondary: 6 month mortality Development of pulmonary hypertension at 6 months RV dysfunction at 6 months Inclusion: Adult patients (≥18 years of age) Confirmed massive PE Massive PE Definition Acute PE with sustained hypotension (SBP 75% lysis of thrombus Complications Post Thrombolysis: Primary Safety Outcome: No major bleeding or stroke observed 3 patients with minor bleeding 2pts with epistaxis (2 days after thrombolysis) 1pt with gingival bleeding (3 days after thrombolysis) All bleeding events occurred during heparin infusion and stopped with gentle compression without recurrence 6pts (17.6%) had major bleeding and 2pts (5.68%) had minor bleeding due to warfarin Strengths: Consecutive patients enrolled which minimizes selection bias All patients followed for 6 months (No loss to follow up) Limitations: Single center, nonrandomized observational trial No comparison group receiving standard therapy (i.e. compared to half-dose 50mg or full dose 100mg of alteplase) Small sample size with few complications makes this an underpowered study to make any firm conclusions about bleeding risks Lots of missing methodology Unclear what time period patients were recruited How strict were authors in consecutive recruitment (? selection bias) Unclear therapies prior to lytics (i.e. Pressors, heparin, etc) Who performed echos and unclear degree of consistency (Echo has some subjectivity to it) Discussion: PE is a Spectrum of Disease Massive PE is also a spectrum of disease This study doesn’t appear to include critically ill massive PE patients who are peri-arrest Dripping alteplase over 6 hours is most likely not going to be the appropriate therapy in the more severe massive PE patients Primary Efficacy Outcome Multiple primary efficacy outcomes were listed in this study, which can be problematic when you get multiple outcomes of varying statistical significance. In this trial all the primary efficacy outcomes were statistically significant, and the authors clearly defined what they meant by complete success in this trial Complications While in Hospital No cases of major bleeding or ICH in this study The 3 patients who had minor bleeding at 48 to 72hrs were most likely due to the heparin infusion and not associated with thrombolysis The cohort is simply too small with not enough complications for the study to be powered correctly for this outcome IV Access These authors gave alteplase through a peripheral IV which we do in stroke patients, but that is typically done over 1hr not over 6hrs If I was going to do this (25mg alteplase over 6hrs) I would want a central venous catheter to avoid the potential of infiltration or if the patient decompensates further and needs central venous access after the fact there is a higher risk of hematoma/bleeding Also, I would already have an arterial line in place before starting thrombolysis for continuous hemodynamic monitoring Heparin Dosing Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed Prior studies have found marked increase in bleeding when lytics and heparin are given together After thrombolysis I typically don’t bolus heparin and just start the infusion Also I don’t start the heparin infusion immediately after thrombolysis, I wait for the PTT to be 2x the control before starting A dose of 0.5 to 4.0mg/hr typically given in EKOS therapy (See Below). This trial gave 25mg over 6hrs (≈4mg/hr) ULTIMA Trial [5]: 59pts with massive/submassive PE Used alteplase at a dose of 1mg/hr x5hrs, then 0.5mg/hr x10hrs Max Dose ≈20mg No major bleeding SEATTLE II Trial [6]: 150pts with massive/submassive PE Used alteplase at a dose of 1mg/hr x24hrs Max Dose ≈25mg 1 severe/life-threatening hemorrhage (Groin hematoma requiring vasopressor support) No ICH OPTALYSE-PE Trial [7]: 101pts with submassive PE Used alteplase at a dose of 8mg/2hrs (4mg/hr), 8mg/4hrs (2mg/hr), 12mg/6hrs (2mg/hr), and 24mg/6hrs (4mg/hr) Max Dose 24mg No major bleeding with 8mg/2hrs, 8mg/4hrs, and 12mg/6hrs 2 major bleeding episodes occurred in the 24mg/6hr group The max dose any patients got was ≈25mg (Max Dose Range ≈20mg to ≈25mg). Major bleeding seemed to occur in the drips that ran for over 15hrs (3 pts out of 310 [≈1%]); But no cases of major bleeding for drips ≤15hrs To take this one step further this trial raises the question of whether EKOS even necessary or is it an overly expensive intervention that potentially increases complications without improving outcomes? Although this was not a randomized clinical trial and there was no comparator arm we do have two trials on submassive PE with half-dose alteplase (50mg) given over 2hours [8] and half-dose alteplase (50mg) given in Massive PE [3] MOPETT Trial [8] 121pts with submassive PE (Called “moderate PE” in the study) Randomized to half dose thrombolysis vs anticoagulation alone For patients weighing ≥50kg a total dose of 50mg given (10mg bolus by IV push followed by 40mg infusion over 2hrs) For patients weighing 50kg a total dose of 0.5mg/kg given (10mg bolus by IV push followed by the remainder over 2hrs) Primary endpoints consisted of pulmonary HTN and composite of pulmonary HTN and recurrent PE at 28mos Pulmonary HTN at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone Composite Pulmonary HTN and Recurrent PE at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone There were 0 cases of bleeding in either arm PEAPETT Trial [3] 23 patients with PEA cardiac arrest due to confirmed massive PE All pts received 50mg of alteplase as an IV push while CPR was ongoing ROSC occurred in 2 to 15 min after alteplase administration in all but one patient There was no minor or major bleeding despite chest compressions What this current trial [9] is really adding to the literature is an even lower dose of thrombolysis (25mg) efficacious? We already know from the MOPETT trial [8] and PEAPETT trial [3] that half-dose alteplase (50mg) had zero cases of bleeding so this current trial just tells us what we already know. 25mg of alteplase has less risk of bleeding than 50mg of alteplase Additionally, if 25mg can treat massive PEs [9], this could also be extrapolated to less severe high-risk submassive PEs (Although I would still love to see a head-to-head trial of 25mg vs 50mg) Author Conclusion: “Results of this pilot study suggest that low-dose prolonged infusion of tPA is an effective and safe therapy in patients with massive PE. This protocol was also effective in decreasing PASP and restoration of RV function.”  Clinical Take Home Point: Low dose (25mg) alteplase given as a prolonged infusion (over 6hrs) is a promising effective and safe therapy in patients with massive PE and provides an alternative to full dose (100mg) and half-dose (50mg) alteplase. Larger RCTs comparing doses of alteplase are warranted to confirm these findings. References: Jaff MR et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement from the American Heart Association. Circ 2011. PMID: 21422387 Wan S et al. Thrombolysis Compared with Heparin for the Initial Treatment of Pulmonary Embolism: A Meta-Analysis of the Randomized Controlled Trials. Circ 2004. PMID: 15262836 Sharifi M et al. Pulseless Electrical Activity in Pulmonary Embolism Treated with Thrombolysis (from the “PEAPETT” Study). AJEM 2016. PMID: 27422214 Wang C et al. Efficacy and Safety of Low Dose Recombinant Tissue-Type Plasminogen Activator for the Treatment of Acute Pulmonary Thromboemolism: A Randomized, Multicenter Controlled Trial. CHEST 2010. PMID: 19741062 Kucher N et al. Randomized, Controlled Trial of Ultrasound-Assisted Catheter-Directed Thrombolysis for Acute Intermediate-Risk Pulmonary Embolism. Circ 2014. PMID: 24226805 Piazza G et al. A prospective, Single-Arm Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism: The SEATTLE II Study. JACCC Cardiovasc Interv 2015. PMID: 26315743 Tapson VF et al. A Randomized Trial of the Optimum Duration of Acoustic Pulse Thrombolysis Procedure in Acute Intermediate-Reisk Pulmonary Embolism: The OPTALYSE PE Trial. JACC Cardiovasc Interv 2018. PMID: 30025734 Sharifi M et al. Moderate Pulmonary Embolism Treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol 2013. PMID: 23102885 Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358 For More Thou

    28 min
  5. 07/02/2024

    REBEL Core Cast 117.0 – Infections of Pregnancy

    Take Home Points Infections are a leading cause of maternal mortality worldwide. Prompt recognition is critical in management. Most infectious processes will require admission and close observation for improvement or decompensation. REBEL Core Cast 117.0 – Infections of Pregnancy Click here for Direct Download of the Podcast Urinary Tract Infection/Pyelonephritis Epidemiology: Occurs in as many as 15% of pregnant women and between 20-40% of pregnant women with asymptomatic bacteriuria will progress to pyelonephritis (Gorgas 2008) Management: Uncomplicated UTI Suggested antibiotics include: Nitrofurantoin 100mg PO BID x7 days OR Cephalexin 500mg PO BID x7 days Pyelonephritis Hospital admission Suggested antibiotics include: Ceftriaxone 1g IV Q24H OR Aztreonam 2g IV Q8H for beta-lactam allergy Complications: Maternal sepsis Maternal renal injury Congenital abnormalities of the fetus Premature rupture of membranes Low birth weight Chorioamnionitis Definition: Also known as intraamniotic infection.  Chorioamnionitis is a bacterial infection of fetal amnion and chorion membranes. Epidemiology: Occurs in 1 to 10% of all pregnancies (Gorgas 2008) Incidence increases significantly with preterm labor Diagnosis: Chorioamnionitis is defined as maternal fever >38°C and at least two of the following (Apantaku and Mulik 2007): Maternal tachycardia >100 beats/min for five minutes Fetal tachycardia >160 beats/min for five minutes Purulent or foul-smelling amniotic fluid or vaginal discharge Uterine tenderness Maternal leukocytosis Evaluation (Abbrescia 2003): CBC Blood cultures Vaginal fluid for phosphatidylglycerol Tests for fetal lung maturity Cervical AND vaginal cultures Physical Exam Avoid digital cervical exam Speculum exam should be done with sterile speculum Ultrasonography for fetal well being Management: Given concern for neonatal sepsis, patients should be admitted for IV antibiotics, supportive cares, and possible early delivery Most commonly an ascending infection from normal vaginal flora, so antibiotics must be chosen to cover polymicrobial infections Ex. Ampicillin IV 2g Q6H AND Gentamicin IV 1.5mg/kg Q8H In PCN allergic patient substitute vancomycin 1 g IV Q12H for ampicillin Can only be considered cured with delivery of infected products of conception Complications: Placental abruption Premature birth Neonatal sepsis Neonatal death Cerebral palsy Maternal sepsis Need for cesarean delivery Postpartum hemorrhage Postpartum Endometritis Definition: Generalized uterine infection Epidemiology: Sepsis results in 15% of maternal deaths worldwide (Houry 2014) More common in surgical than vaginal deliveries May co-exist with surgical site infection Diagnosis: Classic triad includes: fever, lower abdominal pain and uterine tenderness, and foul smelling lochia Management: Hospital admission Cover for polymicrobial infection, including anaerobes Ex. Clindamycin 900 mg IV Q8H AND Gentamicin 5-7 mg/kg IV Q24H Septic Abortion Epidemiology: The World Health Organization estimates that one in eight pregnancy related deaths worldwide can be directly attributed to unsafe abortion procedures (Gorgas 2008) Diagnosis: Clinical presentation includes fever, abdominal pain and uterine tenderness in setting of recent abortion Presentation can vary from mild infection to septic shock Evaluation: Lactate Cultures of cervix, blood and urine Coagulation panel to screen for DIC Abdominal X-ray to evaluate for free air or retained surgical foreign bodies Pelvic ultrasound to evaluate for retained products of conception or surgical foreign bodies Management: Hospital admission may be indicated as infection can progress to septic shock, organ failure, DIC and cardiovascular collapse Broad-spectrum antibiotics are indicated.  Triple antibiotic coverage is recommended.  Suggested regimens include: Ampicillin AND Gentamicin AND Clindamycin OR Metronidazole Update tetanus vaccination Usually requires dilation and curettage to remove any retained products of conception or foreign bodies. References: Abbrescia, K. and B. Sheridan (2003). “Complications of second and third trimester pregnancies.” Emerg Med Clin North Am 21(3): 695-710, vii. PMID: 12962354 Apantaku, O. and V. Mulik (2007). “Maternal intra-partum fever.” J Obstet Gynaecol 27(1): 12-15. PMID: 17365450 Desai, S. and S. Henderson. Labor and Delivery and Their Complications. In: Marx, J et al, ed. Rosen’s Emergency Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014:2331-2350. Gorgas, D. L. (2008). “Infections related to pregnancy.” Emerg Med Clin North Am 26(2): 345-366, viii. PMID: 18406978 Houry, D and B. Salhi. Acute Complications of Pregnancy. In: Marx, J et al, ed. Rosen’s Emergency Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014: 2282-2299. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 117.0 – Infections of Pregnancy appeared first on REBEL EM - Emergency Medicine Blog.

    5 min

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Rational Evidence-Based Evaluation of Literature

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