Multifocal opacities…

A patient presented to the ED with flu-like symptoms in the height of flu season:

multifocal opacities

Chest CT:

Multifocal opacities CT 2 Multifocal opacities CT

The CT demonstrates multifocal opacities with some cavitation on the larger lesions.  There seems to be a peripheral and lower-lobe predominence.  This could represent atypical pneumonia (legionella, mycoplasma, chlamydia), fungal pneumonia (cocciodomycosis, histoplasmosis, aspergillosis), miliary tuberculosis, metastatic lesions or carcinomatosis, septic emboli, or viral pneumonia.

After a significant inpatient workup the final diagnosis was Human Metapneumovirus.  All others were ruled out and viral testing revealed this culprit.

Image contributors:  David Barnes, MD and Julie Phan, MD

Author:  Russell Jones, MD


Filed under: Chest, Chest XR, CT, Non-Trauma, Respiratory, XR Tagged: Pneumonia

Hip Ultrasound and Arthrocentesis

General Info/Intro

Bedside ultrasound can be used to evaluate and diagnose hip effusions when concerned for septic joint. It is both effective in visualizing an effusion and assisting in arthrocentesis.1 Emergency physicians with ultrasound training have been shown to be capable of visualizing effusions of the hip with a sensitivity between 80-85% and specificity between 98-100%.2

Diagnosis

  • Orient curvilinear probe with the indicator toward the patient’s umbilicus (approximately 30 degrees off axis of the femoral shaft)
  • Locate femoral head and neck and measure the largest fluid collection
  • >5mm effusion or >2mm effusion compared to healthy side = positive finding

Procedure

  • Use sterile probe cover and sterile technique
  • Orient needle in long axis (parallel to the probe) to visualize the entire shaft during aspiration
  • Common labs include cell count with diff, gram stain, and culture (most important)

Recap

  • Orient probe marker to umbilicus
  • Effusion >5 mm or a difference >2 mm from asymptomatic contralateral side = positive finding

Bottom Line/Pearls & Pitfalls

  • No fluid does not necessarily mean a negative septic joint

Figures

Normal sonographic hip

Normal sonographic hip

Positive joint effusion

Positive joint effusion

Further Reading / References

  1. Marx, J., Hockberger, R., Walls, R. (2013). Rosen’s Emergency Medicine- Concepts and Clinical Practice (8th ed., pp. 1845). Philadelphia, PA: Elsevier.
  2. Vieira R, Levy, J. Bedside Ultrasonography to Identify Hip Effusions in Pediatric Patients. Ann Emerg Med. 2010; 55:284-289.
  3. Reynolds, J., Euerle, B. Images in Emergency Medicine. Ann Emerg Med. 2011; 57: e18-e19.
  4. http://www.ncbi.nlm.nih.gov/pubmed/23960065
  5. http://www.ncbi.nlm.nih.gov/pubmed/22942931
  6. http://www.ncbi.nlm.nih.gov/pubmed/22284975
  7. http://www.ncbi.nlm.nih.gov/pubmed/18403170
  8. http://www.ncbi.nlm.nih.gov/pubmed/17157689
Edited by Alex Koyfman

The post Hip Ultrasound and Arthrocentesis appeared first on emDocs.

Senior Report 7.12

Case Presentation by Dr. Megan Dougherty, MD

CC: unable to obtain due to clinical condition

HPI: The patient is a 19 years old male presenting to the ED from county jail for altered mental status. The patient has been in county jail for 5 days. He has a known history of psychiatric disease for which he was possibly given valproic acid (records are unclear). Per the officer escorting the patient, the patient has eaten or drank anything in several days and was found moaning on the floor shaking prior to arrival and that is why he is at the hospital.

ROS:
Unable to obtain due to clinical condition

Past Medical History:  Psychiatric disease
Surgical history:  Unknown
Allergies:  None known
Medications:  Possibly valproic acid administered at the jail, but no officer was able to verify if and or what medications were administered daily
Family history:  Unable to be obtained
Social history:  Currently in county jail. Unclear as to whether the patient smokes tobacco, uses alcohol or illicit drugs.

Physical exam:
Vitals:  Temperature: 39.2, blood pressure: 189/122, heart rate 154, respiratory rate 27, pulse oximetry 92% on room air
Appearance: in acute distress, shaking all four extremities and looking at everyone in the room, moaning
Mental status: making good eye contact, does not speak but continues to moan
Eyes: Pupils are equal and are 4 mm.
HENMT: head: normocephalic, atraumatic. Nose: no nasal discharge or epistaxis. Mouth: mucous membranes are dry and chapped. Throat: mildly erythematous, no tonsillar hypertrophy
Cardiovascular: tachycardic, regular rhythm. There is a good S1 and S2 without any murmurs. 2+ pulses are felt in all extremities. There is no lower extremity edema.
Respiratory: Clear to auscultation bilaterally. There are no wheezes or crackles. The patient is mildly tachypneic but there are no retractions. The patient is moaning.
Abdomen: soft, non tender to palpation. There is no guarding or rigidity
Musculoskeletal: moving all four extremities. There is no tenderness to palpation of any joint.
Neurological: The patient does not follow commands. He has no facial asymmetry. He continues to have rhythmic jerking. He continues to moan incoherently. Patellar and biceps DTRs are 3+ bilaterally. There is no clonus.
Skin: hot and dry. There is no abrasion or rash.

EKG was obtained. It showed sinus tachycardia. Labs were sent. A CT of the head and a chest x-ray were ordered. The patient was given 4 mg of Ativan for agitation. The patient was also given four liters of fluid. He was given 650 mg of acetaminophen rectally.

After you return to the module, you get a call from radiology to come to their lair to help interpret the head CT. This is what they show you.

megan

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Questions:

1. Based on this imaging, what other imaging do you need?
A. soft tissue neck
B. CT neck
C. chest x-ray
D. CT thorax

2. What is the likely source of the subcutaneous emphysema?
A. CPR
B. pneumothorax
C. necrotizing fasciitis
D. injection drug use

3. If imaging modalities chosen do not show source of subcutaneous emphysema, what is the next step?
A. place chest tube
B. consult neurosurgery
C. consult the ICU
D. consult ENT

 

ANSWERS:

  1. C – Chest x-ray- Most common source of subcutaneous emphysema is from the chest.
  2. B – Pneumothorax
  3. D – Consult ENT- In the event that no obvious source is found on imaging, the next step would be evaluation of the airway for defects causing the subcutaneous air. ENT did scope the patient in the case and there was no source of the subcutaneous air found in the airway.

While the etiology of this patient’s alteration was not elucidated by the workup performed, the subcutaneous emphysema was cause for alarm for further workup into potential causes that may not have provided a unifying diagnosis. Certainly, infection, ammonia, NMS, or serotonin syndrome, and others were all a consideration in this altered, febrile patient with a history of psychiatric disorder.

Subcutaneous emphysema:
Subcutaneous emphysema was first described in 1850, as a complication of a patient with asthma.   Subcutaneous emphysema and pneumomediastinum are both known complications of asthma.   First descriptions were by Dr. Laennec (who is known as the father of the stethoscope and was the authority on heart and lung sounds in his time) and also by Dr. Hamman. Most common cause of subcutaneous emphysema in modern days is found to be a pneumothorax and/or a chest tube that has become clogged.

Clinical findings of subcutaneous emphysema include soft tissue swelling as well as crepitus to palpation of affected areas. The crunch felt on palpation is sometimes describes as “rice krispies”. This emphysema is typically painless. The subcutaneous emphysema can spread along the soft tissue planes and can extend up to the neck and head if the chest is the primary source. If severe, the subcutaneous emphysema can cause compression of the upper airway and can also cause jugular venous compression. This can lead to airway compromise and possibly cardiovascular compromise. The patients can develop dysphonia and dysphagia when the subcutaneous air dissects into the tissues of the neck. In the most severe cases, the subcutaneous emphysema can be a cause of dyspnea and they may require a tracheostomy. If pneumomediastinum is present, auscultation of heart sounds will reveal Hamman’s sign (or Hamman’s crunch), which is heard on auscultation with heart, sounds a crunching or crackle sound. Pneumomediastinum also typically presents with severe chest pain.

Dr. Hamman first identified the presence of pneumomediastinum in postpartum women; hence Hamman’s sign is heard when there is pneumomediastinum. The pneumomediastinum is likely related to the increased intrathoracic pressure generated when the women is in labor.

There are many case reports of subcutaneous emphysema and pneumomediastinum. Most commonly reported are causes associated with positive pressure ventilation and those following tooth extraction, especially in musicians. Causes of subcutaneous emphysema include but are not limited to: labor and delivery, SCUBA diving, excessive phonation, excessive blowing, positive pressure ventilation, Valsalva type maneuver, asthma, pneumonia, bronchiolitis, tooth extraction, digestive tract surgery IVDA, necrotizing fasciitis, trauma including GSWs and stabbings. When no source of subcutaneous emphysema is found, called spontaneous subcutaneous emphysema. Careful investigation is warranted first before declaring spontaneous subcutaneous emphysema. CT Thorax is helpful in identifying sources in airway or GI tract. If imaging modalities do not show a source, it would be reasonable to have ENT scope the patient to evaluate the airway for any defects.

Management of subcutaneous emphysema is primarily supportive. Treatment of causes such as pneumothorax is warranted. There are case studies of treatment of severe subcutaneous emphysema with bilateral infraclavicular incisions down to the subcutaneous tissue that helps to provide a tract for the air to drain. There are also case reports of placing a subcutaneous drain.

 

References

Chotirmall, SH, Morgan, RK. (2014) Subcutaneous emphysema, BMJ Case Reports. doi: 10.1136/bcr-2013-20112 

Choo, M, Shin S, Kim J. (1998) A Case of Spontaneous Cervical and Mediastinal Emphysema. J. Korean Medical Society, 13: 223-6.

O’Reilly, P, Chen, HK, Wiseman, R. (2013) Management of extensive subcutaneous emphysema with a subcutaneous drain. Respiratory Case Reports, 1(2): 28-30.

 

Roquin, A. (2006). Rene Theophile Hyacinthe Laennec (1781-1826): The Man Behind the Stehoscope. Clinical Med


Filed under: Senior Report

ICTUS 2º a DREPANOCITOSIS. Caso clínico presentado por ANA RENGIFO (R2)

* Datos del paciente: Mujer de 36 años. Origen Nigeriano. Nacionalizada en España hace 15 años.
* Antecedentes Personales: No HTA, No DM, No dislipidemia. Anemia en seguimiento por MAP. Exfumadora desde hace 2 años de 30 cigarros/ día x 6 años.
* Tto. habitual: No refiere ningún tratamiento.
* Motivo de Consulta: Vómito y diarrea.
* Anamnesis: Paciente que no habla castellano, su esposo hace de traductor. Refiere cuadro clínico de 6 horas de evolución de malestar general, sensación de debilidad generalizada que le dificulta levantarse sin ayuda. Inicia con deposiciones líquidas sin productos patológicos,  con vómito bilioso, sin dolor abdominal, fiebre ni otros síntomas asociados.
* Exploración física: Mujer de raza negra que precisa ayuda para deambulación, de buen aspecto general.PA 110/70 mmHg FC 80 lpm Tº 35.9ºC SaO2 97 % (Basal). No IY. No soplo carotideo. Mucosas secas. AC: Ruidos cardiacos rítmicos sin soplos. AP: Campos pulmonares bien ventilados sin ruidos sobreagregados. Abdomen: Blando depresible no se palpan masas ni megalias, sin dolor a la palpación ni signos de peritonismo, peristaltismo aumentado. Extremidades: No edema, no signos de TVP. Exploración Neurológica: dificultad en la exploracion de funciones mentales superiores por idioma. Discreta claudicación de extremidades superior e inferior izquierdas. Reflejos osteotendinosos conservados. Babinski izquierdo. Dismetria en prueba dedo-nariz y talón-rodilla (hemicuerpo izquierdo). No déficit sensitivos. Pares craneales: MOE normales, no nistagmus. Desviación de la comisura labial hacia la derecha. Campimetría por confrontación normal. Resto pares craneales sin alteraciones. Marcha con lateralización izquierda que no corrige.
Pruebas complementarias : EKG: Ritmo sinusal 81 lpm,sin alteraciones de la repolarizacion. Bioquímica: Función renal normal Cr 0.71 urea 23 / Iones normales / Glucosa 140. Hemograma: Leucocitos y formula normales / Ligera anemia normocitica: Hb 11.3, VCM 85  / Trombocitopenia: 62.000 plaquetas / Coagulación normal: INR 0.96.  TAC CEREBRAL: Imagen hipodensa que afecta el núcleo lenticular y capsula interna en relación con lesión isquémica aguda.
* Diagnóstico de presunción: Código ICTUS / Trombocitopenia.
* Tratamiento: Se comenta con servicio de Neurología y se procede a traslado al Hospital de referencia: H.U.Donostia- Unidad de ICTUS.
* Evolución: Paciente en Unidad de Ictus se completa estudio para establecer etiología. En el ingreso hay empeoramiento de la hemiparesia Izquierda con secuelas residuales. Ecografía Duplex TSA y Transcraneal: No se aprecian estenosis significativas, flujos simétricos.  Angio TAC de TSAO: Sin alteraciones significativas en sus trayectos.  Ecografía Abdominal: Esplenomegalia. Estudio de Holter ECG: sin alteraciones.  Estudio de Trombofilia: Anticoagulante lupico Negativo; Proteína C 117%; Proteína S activada; Plasminogeno Normal; ANA Positivos 80, demás ACs Negativos. Mutación del factor II Ausente. Serologías para virus Negativos. Estudio de Hb: Hb A2: 35 % (2.2-3.5) Hb Fetal 4.9 % (0-1). Electroforesis de Hb: Hb S 45% y Hb C 43 % (confirmada). Interconsulta con HEMATOLOGIA: Valorada paciente con resultados de analítica posiblemente se trata de una variante de drepanocitosis. Una hemoglobinopatía SC tiene curso clínico más leve que la Hb SS, Explicaría la esplenomegalia y la trombocitopenia. Iniciar tratamiento: Terapia transfusional crónica/Hidroxiura. Programar vacunaciones. Estudio familiar.
* Diagnóstico final: INFARTO CEREBRAL en ganglios de la base y capsula interna del lado derecho en relación a DREPANOCITOSIS.

 

Señala los motivos por los cuales has elegido presentar este caso clínico (caso de difícil diagnóstico, problema social,…):- El primero es resaltar la importancia del examen físico utilizado como herramienta para reconocer normalidad y/o detectar la presencia de signos que identifican enfermedad, éste es un buen ejemplo. Había límites en la comunicación por idioma, el motivo de consulta (vómitos y diarrea) era el menos importante al curso clínico de la paciente.- Y el otro es como enfermedades como la anemia drepanocitica, pueden pasar sin ser diagnosticadas teniendo complicaciones de gran impacto para la paciente.

DrepanocitosisCOMENTARIO: cuando Ana Rengifo me comentó el caso me pareció interesante, pero tengo que reconocer que mi conocimiento sobre la Drepanocitosis es muy escaso: me suena de lejos su relación con la Anemia Falciforme y con cierto grado de protección contra la malaria, poco más.

Pienso que uno de los aspectos más estimulantes de nuestra labor es poner en evidencia nuestras lagunas de conocimiento e intentar corregirlas. Es la mejor receta contra el BURNOUT = síndrome del quemado. Bueno también puede ocurrir un efecto contrario: que el tema nos resbale y se refuerce nuestro burnout.

Aproximadamente un 5% de la población mundial es portadora de genes causantes de hemoglobinopatías, entre las que destacan la drepanocitosis y la talasemia.


There’s Been A Drive-By Lysing!

If you’ve been keeping up, a couple weeks ago JAMA had a theme issue for Neurology – which nowadays, apparently, is mostly tPA.  And, the latest and greatest – concierge Neurology!  In which they come to your house to give you lytics.

This is the Prehospital Acute Neurological Treatmentand Optimization of Medical care in Stroke Study (PHANTOM-S), conducted in Berlin, Germany, using the Stroke Emergency Mobile (STEMO) vehicle.  They compared time-to-thrombolysis during 46 weeks of standard care with 46 weeks of STEMO period – and, within STEMO period, operation of the vehicle was a week-on/week-off deployment.  Unsurprisingly, driving the tPA to the patient shaves 25 minutes off the alarm to tPA time.  Success!

MedPage Today, with it’s usual insightful analysis, breaks out a table of glowing secondary outcomes – improvements in in-hospital all-cause mortality, discharge to home, symptomatic intracranial hemorrhage, and overall tPA complications …

… before acknowledging all these improvements occurred even when the STEMO wasn’t deployed, and it was rather general stroke care improvements over the study period reflected in these secondary outcomes.  Additional praise is provided by James Grotta, who has started his own mobile stroke unit in Houston.  And, finally, Associated Editor Jeff Saver, of endless tPA conflict-of-interest disclosures, chimes in for the Editor’s audio summary.

I think it’s clear, between this and its preceding pilot study, that it is possible to drive a bus around with a stroke neurologist and a CT scanner and rule out intracranial hemorrhage.  The main concern might be over-treatment of stroke mimics, but these authors state the same number of patients treated in all observation windows ultimately received non-stroke diagnoses.  However, they report a baseline stroke mimic treatment rate of 2.2% – which is line with other literature describing institutions that don’t go looking very hard for non-stroke diagnoses after tPA.  Other institutions that require MRI signs of ischemic lesions have stroke mimic rates up to 15.5%, so I wouldn’t place much stock in this specific statistic as a measure of quality.

The last issue – a reasonable case can be made for safety as long as there’s a neurologist riding shotgun in the ambulance.  However, you’ll have to find neurologists willing to take such emergency call and support their salaries while they wait for deployment, which will end up being logistically and financially unworkable.  The next step, I presume, will be pre-hospital telestroke where paramedics are supervised by a remote neurologist.  A bright, or dim, future, depending on your view of tPA.

“Effect of the Use of Ambulance-Based Thrombolysis on Time to Thrombolysis in Acute Ischemic Stroke”
http://jama.jamanetwork.com/article.aspx?articleid=1861800

There’s Been A Drive-By Lysing!

If you’ve been keeping up, a couple weeks ago JAMA had a theme issue for Neurology – which nowadays, apparently, is mostly tPA.  And, the latest and greatest – concierge Neurology!  In which they come to your house to give you lytics.

This is the Prehospital Acute Neurological Treatmentand Optimization of Medical care in Stroke Study (PHANTOM-S), conducted in Berlin, Germany, using the Stroke Emergency Mobile (STEMO) vehicle.  They compared time-to-thrombolysis during 46 weeks of standard care with 46 weeks of STEMO period – and, within STEMO period, operation of the vehicle was a week-on/week-off deployment.  Unsurprisingly, driving the tPA to the patient shaves 25 minutes off the alarm to tPA time.  Success!

MedPage Today, with it’s usual insightful analysis, breaks out a table of glowing secondary outcomes – improvements in in-hospital all-cause mortality, discharge to home, symptomatic intracranial hemorrhage, and overall tPA complications …

… before acknowledging all these improvements occurred even when the STEMO wasn’t deployed, and it was rather general stroke care improvements over the study period reflected in these secondary outcomes.  Additional praise is provided by James Grotta, who has started his own mobile stroke unit in Houston.  And, finally, Associated Editor Jeff Saver, of endless tPA conflict-of-interest disclosures, chimes in for the Editor’s audio summary.

I think it’s clear, between this and its preceding pilot study, that it is possible to drive a bus around with a stroke neurologist and a CT scanner and rule out intracranial hemorrhage.  The main concern might be over-treatment of stroke mimics, but these authors state the same number of patients treated in all observation windows ultimately received non-stroke diagnoses.  However, they report a baseline stroke mimic treatment rate of 2.2% – which is line with other literature describing institutions that don’t go looking very hard for non-stroke diagnoses after tPA.  Other institutions that require MRI signs of ischemic lesions have stroke mimic rates up to 15.5%, so I wouldn’t place much stock in this specific statistic as a measure of quality.

The last issue – a reasonable case can be made for safety as long as there’s a neurologist riding shotgun in the ambulance.  However, you’ll have to find neurologists willing to take such emergency call and support their salaries while they wait for deployment, which will end up being logistically and financially unworkable.  The next step, I presume, will be pre-hospital telestroke where paramedics are supervised by a remote neurologist.  A bright, or dim, future, depending on your view of tPA.

“Effect of the Use of Ambulance-Based Thrombolysis on Time to Thrombolysis in Acute Ischemic Stroke”
http://jama.jamanetwork.com/article.aspx?articleid=1861800