Approach to ALTE

 A mother brings in a 2 week old neonate with a history choking that said
 morning, turning blue and becoming limp. Same occurred while feeding. No
 other history was elicited.  When examined, neonate had temp of 98 degrees
 Fahrenheit, pulse rate of140 bpm, no other vitals recorded. When examined,
 the child was active, alert and the cardiovascular and abdominal
 examinations were reportedly normal. However, a few crepitations were
 elicited in the left lung base.   How will  you approach this case?

(This article is based on a case posed by Dr.Celeste Maycock,a real advocate of academic excellence) 

 As per definition this neonate fit in ALTE ( Acute Life Threatening Event). ALTE is subjective to care provider but it is important enough to be careful in managing this type of case as well as it is paramount to document care fully. Let us understand component of ATLE:

Frightenning to parents or care provider

blue (cynosis)

limping (loss of tone)

choking (unable to breath)

So this is a case of ATLE

Pt. came : need Red card inside : to be directed to ER: immediate vitals including RBG and SpO2

While looking at neonate place to medium  flow oxygen,Monitor Airway, breathing, circulation (ABCs) with respiratory compromise, establish an airway & provide supportive therapy (e.g., oxygen, mechanical ventilation) Monitor Vital signs

• Establish vascular access for sampling blood ):
• If sepsis is suspected or another specific cause is not identified, start on broad spectrum antibiotics (e.g., ampicillin and gentamycin) after obtaining a CBC, urinalysis, blood & urine cultures (if possible). Left untreated, sepsis may lead to pulmonary disease & left ventricular dysfunction.
• Administering meds (if needed.  kept on talking with mother and get all information from the mother  ante natal,perinatal including baby's last 2 week (for this case):

Now go for differential  one by one for  each component of ALTE

CYNOTIC:

Pregnancy HX ___>  Associated causes of cyanosis

• Gestational diabetes mellitus (GDM) -->TTN (ransient tachypnea of the newborn) (, RDS, hypoglycemia, TGA
• Oligohydramnios-->Pulmonary hypoplasia
• Pregnancy induced hypertension -->IUGR, polycythemia, hypoglycemia
• Lithium intake (1st trimester)--->Ebstein’s anomaly
• Advanced maternal age->Trisomy 21 associated with many congenital heart defects (cyanotic and acyanotic)

Labour Hx----> Associated causes of cyanosis

• PROM, fever, GBS +ve -->Sepsis
• Sedatives/anesthetics--->Respiratory depression, apnea
• C-section -->TTN, PPHN (persistent pulmonary hypertension of the newborn)
• Preterm infant-->RDS
• Meconium-->MAS (pneumonia)

   YOUR DIFFERENTIAL STARTS  HERE......MOTHER's HX FIRST

 

Do thorough Physical examination:  I always consider  dealing with neonate is almost a vetrenary practice: Neonate  doesnot say any thing.

 Look at the neonate differentiate cynosis is whether peripheral or central

 Look at the vitals,

     1/signs of respiratory distress : tachypnea, retractions, nasal flaring & grunting usually indicate a respiratory problem

     2/Congenital heart disease : absent or effortless tachypnea.

     3/Sepsis often has the following findings: peripheral cyanosis, HR, Increase  RR, Decrease BP, Increase/Decrease temp (DDX:  left-sided obstructive lesions:  hypoplastic left heart syndrome, critical aortic stenosis & severe coarctation of the aorta).

  4/Rule out choanal atresia.  If in doubt, attempt to insert a catheter through the nares

Listen for murmurs: a systolic murmur audible in most forms of cyanotic CHD (exception:  d-TGA with intact ventricular septum & no pulmonary stenosis).

Assess the abdomen: scaphoid abdomen in diaphgragmatic hernia

Consider neurological disorders: observe for apnea and periodic breathing, which may be related to immaturity of the nervous system.  Seizures can cause cyanosis if the infant fails to breathe during the episodes.

Tracheal atresia with tracheooesophageal connection can give cynosis with feeding effort.

Here it becomes imperative to think about the various mechanism of cyanosis. Then, organize your thoughts by anatomical systems.

Ventilation/perfusion mismatch : delivery

• Airway disease: transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), pneumonia, aspiration (meconium, blood, amniotic fluid), atelectasis, diaphragmatic hernia, pulmonary hypoplasia, pulmonary hemorrhage, CCAM
• Extrinsic compression of the lungs: pneumothorax, pleural effusion, hemothorax,
• Intracardiac: The 5 T’s: Tetralogy of Fallot, Tricuspid atresia, Transposition of the great arteries, Total anomalous pulmonary venous return, Truncus arteriosus; and pulmonary atresia, Ebsteins anomaly (abnormal tricuspid valve), hypoplastic left heart (shunts)
• Great vessel level: persistent pulmonary, hypertension of the newborn
• Intrapulmonary level: pulmonary arteriovenous malformation

Alveolar Hypoventilation

• CNS depression: asphyxia, maternal sedation, intraventricular hemorrhage, seizure, meningitis, encephalitis
• Airway obstruction: choanal atresia, laryngomalacia, Pierre Robin syndrome
• Neuromuscular disease: phrenic nerve inury, neonatal myasthenia gravis

Diffusion Impairment

• Pulmonary edema: left-sided obstructive cardiac disease (aortic stenosis), cardiomyopathy
• Pulmonary fibrosis

Decrease Hemoglobin O2 affinity

• Methemoglobinemia (congenital, drugs)

Decrease Peripheral circulation (peripheral cyanosis)

• Sepsis, shock of any cause, polycythemia, hypothermia, hypoglycemia, low cardiac output (hypocalcemia, cardiomyopathies, etc)

Investigation:

CBC

             Increase or decrease  WBC : sepsis

• Hematocrit > 65% : polycythemia

Serum glucose:

• to detect hypoglycemia

Arterial Blood Gases (ABGs):

• Arterial PO2: to confirm central cyanosis : SaO2 not as good an indicator due to  Increase fetal Hb affinity for O2 (left-shift)
• Increase PaCO2: may indicate pulmonary or CNS disorders, heart failure
• Decrease pH: sepsis, circulatory shock, severe hypoxemia
• Methemoglobinemia: Decrease SaO2, normal PaO2, chocolate-brown blood

Hyperoxia test:

• Administer 100 % oxygen for > 10 min
• PaO2 > 100 mmHg: pulmonary disease likely
• PaO2 < 70 mmHg, rise by < 30 mmHg or SaO2 unchanged:  cardiac cause (R-L shunt) likely
• Total anomalous pulmonary venous return may respond
• Pulmonary disease with a massive intrapulmonary shunt may not respond

Pre-ductal & Post-ductal PaO2 or SaO2 measurements (pre- and post- ductus arteriosus):

• Preductal artery (right radial) PaO2 10 – 15 mmHg > post ductal artery  (umbilical artery line) PaO2 : R – L ductal shunt (e.g., pulmonary diseases, commonly PPHN)
• SaO2 can also be measured (right hand & right or left leg) : significant if > 10-15 % difference.

CXR

          To identify pulmonary causes of cyanosis:  pneumothorax, pulmonary  hypoplasia, diaphragmatic hernia, pulmonary edema, pleural effusion, etc.

• Useful in evaluating congenital heart disease:  e.g., cardiomegaly & vascular congestion: heart failure
  • TGA : egg-on-a-string (anterior/posterior relationship of great vessels)
  • TOF : boot-shaped heart (RVH)
  • TAPVR :  snowman, figure 8 (anomalous drainage chamber in superior mediastinum)

Echocardiography

• Indicated if abnormal cardiac examination suggestive of congenital heart defect, failed hyperoxia test (cardiac disease suspected) or has unclear diagnosis

• An infant who fails the hyperoxia test & does not have PPHN or a CXR showing pulmonary disease likely has a congenital heart defect that’s ductus-dependent.

Limping neonate:

now we have to look into hypotonia of the neonate. At least 35 to 40 differnt conditions can give limp (hypotonia) of muscle but we need to focus which also cause  limping.

Seizure, hypoglycaemia, sepsis  etc.

 

Hypotonia in Neonate and Infants:

Hypotonia is reduced resistance to passive movement of joints. The deficit causing hypotonia originate in the brain, spinal cord, peripheral nerves, neuromuscular junction, and muscle. There are also non-neuromuscular entities that may be associated with hypotonia including:

1.     Prematurity

2.     Hypothyroidism

3.     Rickets

4.     Malnutrition

5.     Kernicterus

6.     Storage diseases

7.     Down Syndrome

8.     Sepsis

9.     Congestive Heart failure

10.  Hypoglycemia

The differential diagnosis of hypotonia is organized anatomically in to central and peripheral causes. Peripheral hypotonia is further divided into disorders of anterior horn cells, peripheral nerves, neuromuscular junction, and muscle. In general, a good history, physical examination, and neurologic exam will lead to the diagnosis.

Characteristicshypotonia (60-80% of cases)

History:

·      Seizures

·      Delay in attaining normal milestones

PE:

·      Don’t track visually

·      Fail to imitate facial gestures

·      Lethargic and less alter

·      Hyperactive DTRs, clones, persistence of primitive reflexes

·      Poor head control

Characteristics of Peripheral Hypotonia (15-30% of cases)

History:

·      Normal sleep-wake patterns

·      Feeding difficulties

PE:

·      Responds appropriately to surroundings

·      Profound generalized weakness

·      Absent reflexes

Central Hypotonia

Hypoxic encephalopathy (19% of cases)

Intracranial hemorrhage

Perinatal trauma

Infections – meningitis or encephalitis

Structural abnormalities

Chromosomal and Genetic abnormalities (31%)

·      Tiresome 21 (Downs Syndrome)

o   Characteristic features: hypotonia, mental retardation, and congenital heart defects

o   Dysmorphic features present in neonates: flat facial profile and nasal bridge, short neck with excess uncial folds, single transverse palmer crease, upslanting palpebral fissures

·      Fragile X

o   Genetic defect: expansion of trinucleotide repeat (CGG) on X chromosome

o   Hypotonia is mild and kids are usually diagnosed after failure to meet developmental milestones

o   Characteristic features: mental retardation, autistic features, macrocephaly, large ears, increased testicular size in puberty

·      Prader-Willi syndrome:

o   Characteristic features: hypotonia, hypogonadism, mental retardation, short stature, and obesity

o   Genetic defect: deletion of paternal copy of long arm of chromosome 15q11-13 or maternal uniparental dismay

Now we have differential for both" blue" and "limp" baby  , common are hypoglycaemia, sepsis, seizure, structural abnormalities...  so we need some more data from the docket....proper vitals including  Spo2 & RBG further CBC and routine blood work will help, clinically detailed resp and cvs examination data are important, reflexes should be noted,-----IMPLY PROPER Examination
and documentation.

Emergency Medicine:Accuracy and quality of clinical decision rules for syncope in the emergency department

Ann Emerg Med. 2010 Oct;56(4):362-373.e1.

Accuracy and quality of clinical decision rules for syncope in the emergency department: a systematic review and meta-analysis.

Serrano LA, Hess EP, Bellolio MF, Murad MH, Montori VM, Erwin PJ, Decker WW.

Department of Emergency Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA. serrano.luis@mayo.edu

Abstract

STUDY OBJECTIVE: We assess the methodological quality and prognostic accuracy of clinical decision rules in emergency department (ED) syncope patients.
METHODS: We searched 6 electronic databases, reviewed reference lists of included studies, and contacted content experts to identify articles for review. Studies that derived or validated clinical decision rules in ED syncope patients were included. Two reviewers independently screened records for relevance, selected studies for inclusion, assessed study quality, and abstracted data. Random-effects meta-analysis was used to pool diagnostic performance estimates across studies that derived or validated the same clinical decision rule. Between-study heterogeneity was assessed with the I(2) statistic, and subgroup hypotheses were tested with a test of interaction.
RESULTS: We identified 18 eligible studies. Deficiencies in outcome (blinding) and interrater reliability assessment were the most common methodological weaknesses. Meta-analysis of the San Francisco Syncope Rule (sensitivity 86% [95% confidence interval {CI} 83% to 89%]; specificity 49% [95% CI 48% to 51%]) and the Osservatorio Epidemiologico sulla Sincope nel Lazio risk score (sensitivity 95% [95% CI 88% to 98%]; specificity 31% [95% CI 29% to 34%]). Subgroup analysis identified study design (prospective, diagnostic odds ratio 8.82 [95% CI 3.5 to 22] versus retrospective, diagnostic odds ratio 2.45 [95% CI 0.96 to 6.21]) and ECG determination (by evaluating physician, diagnostic odds ratio 25.5 [95% CI 4.41 to 148] versus researcher or cardiologist, diagnostic odds ratio 4 [95% CI 2.15 to 7.55]) as potential explanations for the variability in San Francisco Syncope Rule performance.
CONCLUSION: The methodological quality and prognostic accuracy of clinical decision rules for syncope are limited. Differences in study design and ECG interpretation may account for the variable prognostic performance of the San Francisco Syncope Rule when validated in different practice settings.
Copyright © 2010 American College of Emergency Physicians. Published by Mosby, Inc. All rights reserved

Emergency Medicine : Predictors of 30-Day Serious Events in Older Patients with Syncope

Study objective

We identify predictors of 30-day serious events after syncope in older adults.

Methods

We reviewed the medical records of older adults (age ≥60 years) who presented with syncope or near syncope to one of 3 emergency departments (EDs) between 2002 and 2005. Our primary outcome was occurrence of a predefined serious event within 30 days after ED evaluation. We used multivariable logistic regression to identify predictors of 30-day serious events.

Results

Of 3,727 potentially eligible patients, 2,871 (77%) met all eligibility criteria. We excluded an additional 287 patients who received a diagnosis of a serious clinical condition while in the ED. In the final study cohort (n=2,584), we identified 173 (7%) patients who experienced a 30-day serious event. High-risk predictors included age greater than 90 years, male sex, history of an arrhythmia, triage systolic blood pressure greater than 160 mm Hg, abnormal ECG result, and abnormal troponin I level. A low-risk predictor was a complaint of near syncope rather than syncope. A risk score, generated by summing high-risk predictors and subtracting the low-risk predictor, can stratify patients into low- (event rate 2.5%; 95% confidence interval [CI] 1.4% to 3.6%), intermediate- (event rate 6.3%; 95% CI 5.1% to 7.5%), and high-risk (event rate 20%; 95% CI 15% to 25%) groups.

Conclusion

We identified predictors of 30-day serious events after syncope in adults aged 60 years and greater. A simple score was able to stratify these patients into distinct risk groups and, if externally validated, might have the potential to aid ED decisionmaking.

Emergency Medicine: AMI

Acute ST Segment Elevation MI

Problem Based Approach

A 65 year old farmer is brought to the local emergency department with his wife by the local police. Apparently he developed a “twinge of chest pain” while shoveling grain 3 hours ago. He insisted on staying at home until “he collapsed on the floor”. Even then, he wanted to stay home and rest, but his wife insisted on calling 119. The call was answered by police department, and a police officer rushed him and his wife to ER at the hospital. At his admission, he states that the pain is “almost gone”-“what a fuss about nothing.” On a history, he tells the ER physician that he smokes two packs of cigarettes daily, that he drinks a goodly amount of beer and that he had been told that his serum cholesterol level is good; the doctor even told him that his was one of the best values he had ever seen for a man his size and age.  On further questioning, he admits to a dull, aching, viselike pain around his chest radiating to the left shoulder. He also discloses that when the pain was at it worse, he experienced nausea and vomiting, must be due to something he ate last night. His wife adds that she has never seen him in so much pain, but he is a “stubborn old goat”

He still insists that it is just a little stomach trouble, but on physical examination he is sweating and diaphoretic. He also vomited twice since coming to ER. His blood pressure is 165/102 mm Hg, and his pulse is 120 irregular. His abdomen is obese. There is no neurological deficit. On Chest examination, bilateral air entry is good and there is no added sound. First and second Heart sound is audible in all auscultatory area and there is no murmur.

Approach

1/ First, ascertain that the patient’s airway is patent (Talk to patient, vomit or any blockage) and administer 100% oxygen.

2/Do an ECG: 

12 lead ECG  

•       The 12-Lead ECG sees the heart from 12 different views.

•     helps you see what is happening in different portions of the heart.

Leads placement

The limb augmented leads “see” electrical activity moving inferiorly (II, III and aVF), to the left (I, aVL) and to the right (aVR).

Precordial leads “see” electrical activity in the  posterior to anterior direction.

Now, using these 3 diagrams let’s figure where to look for a lateral wall and inferior wall MI.

Putting all together: what is it?

Look at again:

Look at some posibilities: 
This patient most likely has suffered an anterolateral wall MI. The history suggest that he is at high risk for infarct and ECG finding confirm the diagnosis.
 An acute inferior wall MI would have ST segment elevation and possible Q wave in the inferior leads. Acute Pericarditis would have ST segment elevation in all leads. Musculoskeletal chest wall pain does not produce the abnormalities in the ECG that are seen in this patient.

Think of thrombolytic therapy:

Thrombolytic therapy should be administered only when the following criteria are met
1/Typical Chest pain suggestive of an Myocardial Infarction
2/ ECG confirming  MI
3/The Absence of other disease that would explain the symptom
Now Look At the Contraindication of thrombolysis:
1/Active internal bleeding
2/Suspected Aortic Dissection
3/Rescent Head Trauma or known intracranial neoplasm
4/Haemorrhaegic Retinopathy
5/Trauma or surgery within the past 2 weeks
6/History of recent(6 months or less) stroke
7/Prolonged or traumatic Cardiorespiratory Resuscitation

How much time you have?:

Greatest Benifit would be acheived if administered thrombolytic therapy within 1-3 hours, but upto 12 hours,10 % mortality benefit can be acheived.

Please note there is no benefit documented for thrombolytic therapy in Non Q wave infarcts, nor for patient with histroy of having Coronary Artery Bypass Graft. 

ADMINISTER FIBRINOLYTIC AGENTS SUCH AS STREPTOKINASE OR ALTEPLASE (t-PA):
Recommended dose:
   1) Streptokinase in AMI : 1.5 million U over 30-60 minutes
   2)Altepase in AMI: 15 mg IV bolus, then o.75 mg/ kg over 30 minutes   (maximum  50 mg), and then o.5 mg/kg for a 60 minute period (maximum 35 mg).


Role of Concomitant Heparin use :

1. In initial treatment of AMI, use of heparin for early and effective anticoaglation  maitains t-PA-induced coronary artery patency more effectively than ASPIRIN alone; high patency result upto 95% were noted in some subgroup analysis.
2. Two most important indications for concomitent use of HEPARIN
           i) acute anterior wall MI
           ii) echocardiographic evidence of left ventricular thrombi
3. It is better to avoid use heparin with streptokinase (except aforesaid indication).
4. Use either low molecular-weight heparin or unfractionated heparin.

ASpirin as ADJUNCTIVE agent:

ISIS-II study showed that ASA reduced mortality by 25%. However,when ASA was added to streptokinase,the effect was synergistic,and mortality from MI was reduced by 42%.

Other modalities of treatment:
Primary Angioplasty with stenting,with addition of glycoprotein IIb/IIIa inhibitor abciximab.

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