Cellulitis Mimics

Introduction
Cellulitis is often misdiagnosed in ED. Available literature reports a misdiagnosis rate of close to 30% that leads to unnecessary admission and antibiotics. 

Cellulitis usually doesn’t affect the deeper layers of skin and presents is a poorly demarcated area of superficial bacterial infection which is painful, erythematous and warm to the touch. It is a clinical diagnosis and no labs are needed unless there are other concerns (Nec Fasc, Osteomyelitis, Abscess). Blood cultures are low yield and should be done only in critically ill and those who fail to improve. Most cases of cellulitis are due to direct inoculation and it is rare for both extremities to be affected at the same time. BILATERAL CELLULITIS IS RARE. Also, cellulitis should be painful rather than itchy. If it is chronic, it is not cellulitis.

Erythema that spreads past drawn margins does not always mean that the patient is worsening. Erythema of cellulitis can spread in the first 48 hours as a normal progression and this does NOT always indicate treatment failure. Think escalation of Antibiotics if erythema is more intense or patient is more ill-appearing or persistent fever.

Common Organisms: Streptococcus pyogenes and Staphylococcus aureas in immunocompetent, without cirrhosis, neutropenia or other risk factors. Purulence or drainage should make you think about staph and consider MRSA in purulent cellulitis if there are risk factors associated. Penicillins or first-generation cephalosporin is a good first choice. Options for MRDA include Sulfamethoxazole/trimethoprim, linezolid, and doxycycline.

(Broad-spectrum antibiotics should be used in critically ill, high risk fo uncommon organismsHigh risk for resistant bacteria)


Mimics

• DVT - Usually differentiable on history and exam
• Stasis Dermatitis - Usually bilateral but can be unilateral as well. Usually due to underlying bilateral venous insufficiency. Leaked out fluid irritates the skin and causes redness. It may be acute (appears and feels as bilateral cellulitis) or chronic (thick hyperpigmented skin with hemosiderin deposits).
• Lipodermatosclerosis. This looks like erysipelas and commonly seen in patients with chronic venous insufficiency. It tends to occur on the medial aspect of the ankle. This can be treated with low dose steroids.
• Necrotising Fasciitis - Pain out of proportion of exam and pain extending beyond the borders of erythema. Most patients are ill-looking with unstable vital signs. Other possible features are insensate skin overlying the area of infection, “Dishwater-appearing fluid” drainage from within the wound. Erythema will often progress rapidly, even within hours. Admit for observation if any concerns for NF. 
• Contact dermatitis presents with pruritis which is a response to an external exposure seen the site of the exposure.
• Dermatohypersensitivity reaction. Allergic-type reaction due to bites, viral infections, medications. 
• Lymphedema, gout and erythema migrans. Usually differentiated based on history
• Calciphylaxis - This is a painful, relapsing and remitting condition which is often seen in cases ofunderlyingg renal failure, diabetes, obesity, liver disease or are taking warfarin. Calcium deposition in blood vessels of the dermis causes skin necrosis and lead to eschars over adipose areas. 

Venous stasis and lymphedema predisposes to cellulitis. 

If on elevating the legs for 1-2 mins, erythema goes away then it is less likely to be cellulitis

Oral v/s IV Antibiotics for Cellulitis

There is good evidence that oral antibiotics are just as good across a wide range of con- ditions such as cellulitis, pneumonia, pyelonephritis, osteomyelitis and even endocarditis. Majority of patients with uncomplicated cellulitis do well with oral antibiotics. 

Take Home

• Think about alternative diagnoses for erythema and warmth
• Bilateral lower extremity cellulitis is rare
• If on elevating the legs for 1-2 mins, erythema goes away then it is less likely to be cellulitis
• When discharging on oral antibiotics, review high risk patients in 48-72 hours 

References:

• Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016; 316(3): 325-37.
• McCreary EK, Heim ME, Schulz LT, et al. Top 10 myths regarding diagnosis and treatment of cellulitis. J Emerg Med. 2017 Oct; 53(4): 485-492.
• Aboltins, CA et al. Oral versus parenteral antimicrobials for the treatment of cellulitis: a randomized non-inferiority trial. J Antimicrob Chemother. 2015 Feb;70(2):581-6.
  PMID: 25336165
  
  
  
  

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       Lakshay Chanana

       

       ST4 Trainee

       Royal Infirmary of Edinburgh

       Department of Emergency Medicine

       Edinburgh

       Scotland

  
  

       @EMDidactic

  
  

  
  

Gullian Barre Syndrome

Guillain-Barré syndrome (GBS) is a heterogeneous group of immune-mediated peripheral neuropathies which presents as evolving polyradiculoneuropathy preceded by a triggering event (often an infection). Cross-reactivity between the pathogen and the nerve tissue sets up the autoimmune response. It typically manifests as a symmetric motor paralysis with or without sensory and autonomic disturbances. The progressive phase of this syndrome is followed by a plateau phase of persistent, unchanging symptoms. Improvement begins within days of the plateau and the time to resolution of symptoms varies among patients.

Patients commonly report a respiratory tract infection or gastroenteritis that resolved when the neuropathy began. Campylobacteriosis is the most common precipitant in GBS.  Other antecedent infections include cytomegalovirus, HIV, Epstein-Barr virus, and varicella-zoster virus.

Typical Presentation

• Weakness (Proximal>Distal, Legs>Arms) accompanied by tingling dysesthesias in the extremities 
• Areflexia few days of symptom onset.
• Cranial nerve involvement may affect airway maintenance, facial muscles, eye move- ments, and swallowing. 
• Shoulder, Back, Thigh Pain (severe, occurring with even the slightest of movements)

The patient with Guillain-Barré syndrome typically presents with weakness accompanied by tingling dysesthesias in the extremities.

Types of GBS
GBS has five distinct subtypes which can be distinguished electrodiagnostically and pathologically. 

1. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)

• Autoimmune disorder, antibody mediated
• Triggered by antecedent viral or bacterial infection Electrophysiologic findings demonstrate demyelination. Inflammatory demyelination may be accompanied by axonal
• nerve loss.
• Remyelination occurs after the immune reaction stops.

2. Acute motor axonal neuropathy (AMAN)

• Pure motor axonal form of neuropathy 
• 2/3rd of patients are seropositive for campylobacteriosis.
• Electrophysiologic studies are normal in sensory nerves
• Reduced or absent in motor nerves. 
• Recovery is typically more rapid. High proportion of pediatric patients

3. Acute motor sensory axonal neuropathy (AMSAN)

• Wallerian-like degeneration of myelinated motor and sensory fibers 
• Minimal inflammation and demyelination
• Similar to AMAN except AMSAN affects sensory nerves and roots 
• Typically affects adults

4. Miller Fisher syndrome

• Rare disorder
• Rapidly evolving ataxia, areflexia, mild limb weakness, and ophthalmoplegia
• Sensory loss unusual, but proprioception may be impaired. Demyelination and inflammation of cranial nerve III and VI, spinal ganglia, and peripheral nerves
• Reduced or absent sensory nerve action potentials, tibial H reflex is usually absent.
• Resolution occurs in one to three months.

5. Acute panautonomic neuropathy

• Rarest of all the variants
• Sympathetic, parasympathetic nervous systems are involved. Cardiovascular involvement is common (postural hypotension, tachycardia, hypertension, dysrhythmias). 
• Blurry vision, dry eyes, anhidrosis, gastrointestinal pseudo-obstruction, and urinary retention 
• Recovery is gradual and often incomplete. 
• Often combined with sensory features

Diagnosis
GBS is the most common type of rapidly evolving, generalized peripheral nervous system disorder. However, there are several mimics that must be considered.

Diagnostic Criteria for Typical Guillain-Barré Syndrome Features required for diagnosis

• Progressive weakness in both arms and legs Areflexia

Features strongly supporting the diagnosis

• Progression of symptoms over days, up to four weeks
• Relative symmetry of symptoms
• Mild sensory symptoms or signs
• Cranial nerve involvement, especially bilateral weakness of facial muscles
• Recovery beginning two to four weeks after progression ceases 
• Autonomic dysfunction
• Absence of fever at onset
• High concentration of protein in cerebrospinal fluid, with fewer than 10 cells per cubic millimeter 
• Typical electrodiagnostic features

Features excluding diagnosis

• Diagnosis of botulism, myasthenia, poliomyelitis, or toxic neuropathy Abnormal porphyrin metabolism
• Recent diphtheria
• Purely sensory syndrome, without weakness

Differential Diagnosis Guillain-Barré Syndrome

• Basilar artery occlusion (asymmetric limb paresis)
• Botulism (descending paralysis)
• Heavy metal intoxication (confusion, psychosis, organic brain syndrome)
• Hypophosphatemia (irritable, apprehensive, hyperventilation, normal cerebrospinal fluid)
• Metabolic myopathies (cerebral and cerebellar symptoms) 
• Myasthenia gravis (weakness and fatigue that improves with rest) 
• Neoplastic meningitis (asymmetric spastic paralysis)
• Neurotoxic fish poisoning (spontaneous recovery within 24 hours) 
• Paraneoplastic neuropathy (chronic)
• Poliomyelitis (purely motor disorder with meningitis)
• Polymyositis (chronic, affects proximal limb muscles)
• Spinal cord compression (asymmetric)
• Tick paralysis (sensory changes absent, normal cerebrospinal fluid) 
• Transverse myelitis (abrupt bilateral leg weakness, ascending, sensory)
• Vasculitic neuropathies (mononeuropathy)

The diagnosis of GBS is based on typical clinical features, electrodiagnostic examination and examination of the cerebrospinal fluid (CSF) can aid in the diagnosis. Characteristic CSF findings consist of elevated protein without pleocytosis (abnormal number of cells in the CSF). 

Treatment
1. Supportive care (Analgesia, Fluids/Electrolytes, Physical Therapy, Nutrition, DVT Prophylaxis, Ventilation)
2. Specific therapy (IVIg, Plasmapheresis)

If patients advance past the acute phase of illness, most will recover function. However, the neuropathy can advance so rapidly that endotracheal intubation and mechanical ventilation may be necessary within 24 hours of symptom onset. Therefore, all patients who have GBS should be admitted to a hospital for close observation for respiratory compromise, cranial nerve dysfunction, and autonomic instability. 

Indications to Consider Intubation

• Forced vital capacity <20 mL per kg
• Maximal inspiratory pressure <30 cm H2O
• Maximal expiratory pressure <40 cm H2O
• Progression is noted with a reduction of more than 30 per cent in vital capacity, maximal inspiratory pressure, or maximal expiratory pressure

Other predictors of subsequent mechanical ventilation:
(1) time from GBS onset to hospital admission of less than seven days
(2) inability to lift the elbows or head above the bed
(3) inability to stand
(4) ineffective coughing
(5) increased liver enzyme levels

Specific treatment should be initiated soon after diagnosis. High-dose intravenous immunoglobulin (IVIg; 400 mg per kg daily for five days) or plasmapheresis can be initiated. IVIg and plasmapheresis are considered as equally effective therapies. 

Disadvantages of plasmapheresis include its rare complications, such as sepsis, that are believed to be caused by depletion of immunoglobulins. If fresh frozen plasma is used as replacement fluid, there is a risk of acquiring viral infections such as hepatitis and HIV. IVIg treatment has advantages over plasmapheresis because it is easier to administer, has significantly fewer complications, and is more comfortable for the patient. 

Despite its benefits, there are side effects from this IVIg therapy such as congestive heart failure and renal insufficiency. Patients may develop fever, myalgia, headache, nausea, and vomiting, but these “influenza-like” symptoms are self-limiting. A history of previous anaphylaxis to IVIg is a contraindication to repeat treatment. 

Corticosteroids were once believed to be useful in the treatment of GBS because of its immune-mediated inflammatory mechanism. However, a Cochrane Database Review of randomized trials, which included 195 patients treated with corticosteroids compared with controls, showed no difference in the outcome. Corticosteroids no longer have a role in GBS treatment.

Approximately 85 per cent of patients with GBS achieve a full and functional recovery within six to 12 months. 

Take Home:

• Guillain-Barré syndrome (GBS) is a heterogeneous group of immune-mediated peripheral neuropathies which presents as evolving polyradiculoneuropathy. It typically presents as Ascending Symmetrical Weakness (Proximal>Distal, Legs>Arms) accompanied by tingling dysesthesias in the extremities, Areflexia, Cranial nerve lesions and Shoulder, Back, Thigh Pain 
• Patients commonly report a respiratory tract infection or gastroenteritis that resolved when the neuropathy began. Campylobacteriosis is the most common precipitant in GBS.  
• Therefore, all patients who have GBS should be admitted to a hospital for close observation for respiratory compromise, cranial nerve dysfunction, and autonomic instability. 
• Treatment of GBS includes Supportive care (Analgesia, Fluids/Electrolytes, Physical Therapy, Nutrition, DVT Prophylaxis, Ventilation) and Specific therapy (IVIg, Plasmapheresis)

References:

• Lindenbaum Y, Kissel JT, Mendell JR. Treatment approaches for Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. Neuro Clin 2001;19:187-204.
• Hughes RA, Wijdicks EF, Barohn R, Benson E, Cornblath DR, Hahn AF, et al. Practice parameter: immunotherapy for Guillain-Barré syndrome: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003;61:736-40.

• Hughes RA, van Der Meche FGA. Corticosteroids for treating Guil- lain-Barré syndrome. Cochrane Database Syst Rev 2003;(4): CD001446. Review.
• Zochodne DW. Autonomic involvement in Guillain-Barré syndrome: a review. Muscle Nerve 1994;17:1145-55
• Newswanger DL, Warren CR. Guillain-Barré syndrome. American family physician. 2004 May 15;69(10).

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Utility of CRP in Emergency Departments

C-reactive protein (CRP) is an acute phase protein synthesized in the liver. It is commonly used in Emergency Departments, especially in febrile and possibly infectious patients. It is also used as a measure of tissue inflammation, a biomarker of disease activity and a prognostic tool of many acute and chronic diseases. CRP functions as a bacterial opsonin, promoting phagocytosis, accelerating chemotaxis, and activating platelets. Normal levels increase with aging. Other possible reasons for higher levels could be:

• Pregnancy
• Coronary Artery Disease
• Viral Infections (10–40 mg/L)
• Bacterial infection (>40mg/dL)
• Malignancy, Obstructive Sleep Apnea, Connective Tissue Disorders

Serial CRP measurements may be helpful to monitor a patient’s response to medical intervention. Although CRP rises with tissue injury or ischemia, in septic patients with fulminant hepatic failure, it is more to be a marker of severe liver dysfunction rather than be used as a marker of infection.

Utility of CRP

1. ACS and Aortic Dissection - For ACS and Dissection, the higher CRP levels, the worse prognosis. It is not used to diagnose ACS/Dissection. Increased CRP levels were independently associated with mortality. 

2. Meningitis - For meningitis, CRP plays a role of distinguishing bacteria from non-bacteria etiology infection.

3. CRP in Acute Abdomen pain
CRP cannot play a suitable role in the diagnosis of cholecystitis but can be a factor indicating the severity of cholecystitis and response to therapy. A normal CRP along with a normal WBC count and a normal neutrophil count is unlikely to be a case of appendicitis. Although early in the course of appendicitis, the white blood cell (WBC) count has shown the best diagnostic sensitivity among laboratory tests, there are 21% of appendicitis is normal levels of WBC count before appendectomy. 

An elevated serum CRP concentration is not accurate in localizing the site of a urinary tract infection in girls who do not have clinical signs of acute pyelonephritis. 

There is no substitute for serial and prudent clinical examinations during an observation period for abdominal pain, especially the initial epigastric pain or peri-umbilical pain.

4. Pnemonia

For pneumonia, CRP plays the roles of prognosis prediction and therapy reflector rather than making diagnosis. CRP is an independent biomarker of severity in community-acquired pneumonia. 

5. Sepsis
Sepsis is a clinical diagnosis and CRP should never used be rule out infection. Procalcitonin has emerged as the most studied and promising sepsis biomarker. For diagnostic and prognostic purposes in critical care, PCT is superior to CRP and other traditional markers of sepsis.


Take Home

In the ED, CRP should not be used to make a diagnosis but to assist evaluation and support your clinical suspicion. In clinically unwell patients, a normal CRP level should never delay antibiotic coverage in ED.  Like other biomarkers, it does not stand alone. In admitted patinets or those on thepary for chronic inflammatory states, CRP can be used for treatment monitoring and severity. 

References

1. Su YJ. The value of C-reactive protein in emergency medicine. Journal of Acute Disease. 2014 Jan 1;3(1):1-5.
2. Rossi E. C-reactive protein and progressive atherosclerosis.Lancet 2002; 360(9344): 1436-1437.
3. Schillinger M, Domanovits H, Bayegan K, Hölzenbein T, Grabenwöger M, Thoenissen J, et al. C-reactive protein and mortality in patients with acute aortic disease. Intensive Care Med2002; 28(6): 740-745.

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Aspiration Pneumonia and Pneumonitis

Aspiration pneumonia (infection occurring from the exposure) results from the swallowing of colonized oropharyngeal contents into the lower respiratory tract with subsequent inflammation and infection. 

Aspiration pneumonitis (Mendelson's syndrome) is from exposure of sterile gastric contents into the lower respiratory tract. This results in a rapid chemical pneumonitis due to irritation of the pulmonary tissues from the acidic material. 

Approximately half of the healthy adults aspirate small amounts oropharyngeal secretions during sleep. Sterile pneumonitis and aspiration pneumonia are difficult to distinguish from one another, even with bronchial lavage. 

Risk Factors for Aspiration

• Reduced Consciousness (EtOH, Drugs, Procedural Sedation, GA)
• Neurologic (Stroke, Seizure, TBI, Dementia, Chronic Neurologic Conditions)
• Oropharyngeal (Poor oral hygiene, Intubation)
• GI (GERD, Esophageal dysmotility, Oral/NG Tube feeding)

About one third of those who aspirate have “silent aspiration” without evidence of cough or gagging. 

Pathophysiology 

• Inflammation (peaks in 4 to 6 hours) --> Increase capillary permeability 
• These reactions may manifest clinically as a cough, pleuritic chest pain, fever, and radiographic findings. 

Typical bacterial species involved in aspiration pneumonia

• S. pneumoniae
• S. aureus
• H. influenzae
• Enterobacteriaceae in community-acquired aspiration pneumonia.

Hospital Acquired Aspiration - P. aeruginosa and gram-negative organisms

Antibiotic therapy for aspiration pneumonia should include coverage for anaerobic organisms.

Presentation

The clinical symptoms of aspiration pneumonia include fever, dyspnea, and productive cough. Patients may show up tachycardia, tachypnea, rales.  Other symptoms of systemic infection in the elderly and debilitated may be present, including a change in mental status, lethargy, and nausea or vomiting.

Witnessed aspiration is a key feature in the diagnosis of aspiration pneumonitis or pneumonia. Typically those with noninfectious aspiration are younger, and the aspiration is witnessed. These patients will present giving a history of aspiration and coughing immediately afterward. 

“Silent aspirators” are typically older and have a chronic neurologic disorder and will present with a cough or fever or general malaise. Historical features that suggest silent aspiration include general debility, recurrent cough, hoarseness, or dysphagia. 


Diagnosis

• CXR usually shows unilateral focal or patchy consolidations in the dependent lung segments (Right lower lobe is the most common in upright aspiration) 
• CT Scan

Initial CXR if done too early in the course may not show any changes

http://www.svuhradiology.ie/case-study/aspiration-pneumonia/

Recumbent Aspiration typically involves posterior portions of the upper lobes and the upper portions of the lower lobes
Upright Aspiration typically involves the most dependent portions i.e. basal segments of the lower lobes. 

Treatment
Large volumes aspiration may require suctioning of the tracheobronchial tree or bronchoalveolar lavage to clear the airway. Bronchodilators aid aspiration-induced bronchospasm.

• Community-Acquired Aspiration (S. aureus, S. pneumoniae, and H. influenzae) - Use Co-Amoxiclav or Levofloxacin
• Suspected MRSA - Add Vancomycin or Linezolid
• Patients with severe periodontal disease, putrid sputum, or lung abscess - Give piperacillin-tazobactam. 

Clinically well-appearing patients with normal gas exchange are candidates for possible discharge with instructions to return if they experience worsening symptoms. Those with significant comorbidities need to get admitted for observation and Antibiotics. 

Further reading

1. Kikuchi R, Watabe N, Komino T, et al: High incidence of silent aspiration in elderly patients with community acquired pneumonia. Am J Respir Crit Care Med 150: 251, 1994. 
2. Marik PE: Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 344: 665, 2001. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @EMDidactic