Algorithm for the Management of Diabetic Ketoacidosis
- American Diabetes Association From Diabetes Care Vol 29, Issue 12, 2006. Modifications from Diabetes Care, Vol 32, Issue 7, 2009.
- WikEM: Diabetic ketoacidosis
64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.
In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.
Non-specific IVCD, LAA, VPC
VT initiated by fusion complex
31F with autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.
In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.
Non-sustained ventricular tachycardia noted on telemetry monitoring
In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others it is of little prognostic significance.6,7,8
|Other||HR > 100||1|
30 year-old female with a history of autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), polysubstance use, brought to the emergency department by ambulance with reported chief complaint of fever. On presentation, the patient reported fever for one day, associated with cough. She was lethargic and confused, answering yes/no questions but unable to provide detailed history. She states that she has been taking her home medications as prescribed, which include hydrocortisone, fludrocortisone, synthroid and insulin. No collateral information was immediately available.
Additional history was obtained from chart review upon discharge. The patient was hospitalized two weeks prior with pneumonia and discharged after two days. For 2-3 days prior to presentation, she reported the following symptoms to family members: nausea/vomiting, cough, decreased oral intake, fevers, and palpitations – she did not take her home medications during this time.
|Gen:||Alert, fatigued, slow responses.|
|HEENT:||No meningeal irritation, dry mucous membranes.|
|Pulmonary:||Tachypnea, inspiratory wheezing and faint crackles at left and right inferior lung fields, appreciated anteriorly as well.|
|Neuro:||Alert, oriented to self, situation, not month/year. PERRL, EOMI, facial muscles symmetric, tongue protrudes midline without fasciculation. Peripheral sensation grossly intact to light touch and moves all extremities on command.|
The patient’s evaluation in the emergency department was concerning for severe sepsis secondary to suspected pulmonary source (given association of fever with cough, hypoxia and abnormal chest imaging findings). The patient had persistent alteration in mental status concerning for CNS infection. While preparing for lumbar puncture, cardiac monitoring revealed sustained polymorphic ventricular tachycardia without appreciable pulse. CPR was initiated, amiodarone 150mg IV push administered and at first pulse check a perfusing sinus rhythm was noted with immediate recovery of prior baseline mental status. Amiodarone load was continued and additional potassium sulfate (PO and IV) was administered. Review of telemetry monitoring revealed preceding 30-45 minutes of non-sustained ventricular tachycardia. The patient had two more episodes of sustained ventricular tachycardia requiring defibrillation. The patient was admitted to the medical intensive care unit for continued management.
#Sustained Ventricular Tachycardia
Initially attributed to critical hypokalemia and hypomagnesemia. However, after appropriate repletion serial ECG’s continued to demonstrate prolonged QT interval (possibly acquired secondary to medications, later review revealed multiple promotility agents for treatment of gastroparesis which could contribute to QT-prolongation including erythromycin and metoclopramide, also associated with endocrinopathies). Early echocardiography demonstrated global hypokinesis with estimated EF 30-35%. This was initially attributed to severe sepsis, as well as recurrent defibrillation. However, cardiac CT after resolution of acute illness showed persistent depressed ejection fraction, no evidence of coronary atherosclerosis. The presence of non-ischemic cardiomyopathy (may be attributable to chronic endocrine dysfunction or prior history of methamphetamine abuse) associated with malignant dysrhythmias warranted ICD placement for secondary prevention which the patient was scheduled to receive.
Attributed to pulmonary source given CT findings, healthcare associated and covered broadly. Mental status gradually improved and returned to baseline. CT head was negative, lumbar puncture deferred.
Unclear etiology. Adrenal insufficiency commonly associated with hyperkalemia and no history of surreptitious fludrocortisone use. Possibly secondary to GI losses. Improved with repletion.
#Autoimmune Polyglandular Syndrome
Started on stress-dose steroids in emergency department. Transiently developed DKA which was reversed appropriately and hydrocortisone was tapered to home regimen. Home levothyroxine was resumed.
|Constitutional||Weight loss, heat intolerance, perspiration|
|Cardiopulmonary||Palpitations, chest pain, dyspnea|
|Neuropsychiatric||Tremor, anxiety, double vision, muscle weakness|
|Neck||Fullness, dysphagia, dysphonia|
|Reproductive||Irregular menses, decreased libido, gynecomastia|
|Vital signs||Tachycardia, widened pulse pressure, fever|
|Cardiovascular||Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur|
|Ophthalmologic||Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze|
|Neurologic||Tremor, hyperreflexia, proximal muscle weakness|
|Dermatologic||Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia|
|Neck||Enlarged or nodular thyroid|
Essentially an exaggeration of thyrotoxicosis featuring marked hyperthermia (104-106°F), tachycardia (HR > 140bpm), and altered mental status (agitation, delirium, coma).
|Moderate (rales, atrial fibrillation)||10|
|Nausea/vomiting, abdominal pain||10|
|Constitutional||Weight gain, cold intolerance, fatigue|
|Cardiopulmonary||Dyspnea, decreased exercise capacity|
|Neuropsychiatric||Impaired concentration and attention|
|Reproductive||Irregular menses, erectile dysfunction, decreased libido|
|Integumentary||Coarse hair, dry skin, alopecia, thin nails|
|Vital signs||Bradycardia, hypothermia|
|Cardiovascular||Prolonged QT, increased ventricular arrhythmia, accelerated CAD, diastolic heart failure, peripheral edema|
|Neurologic||Lethargy, slowed speech, agitation, seizures, ataxia/dysmetria, mononeuropathy, delayed relaxation of reflexes|
|Musculoskeletal||Proximal myopathy, pseudohypertrophy, polyarthralgia|
Either primary due to adrenal gland failure (often secondary to autoimmune destruction), or secondary most often due to exogenous glucocorticoid administration (usually requiring more than 30mg/day for > 3wks).
|Gastrointestinal||Anorexia, nausea, cramping|
|Reproductive||Amenorrhea, decreased libido|
|General||Hyponatremia, orthostatic hypotension, low-grade fever|
|Primary||Hyperpigmentation, hyperkalemia, hyperchloremia, acidosis|
Unfortunately, this patient’s comprehensive clinical picture does not fit neatly into a particular category of endocrinologic pathology. Her underlying autoimmune disorder manifests both primary adrenal and thyroid dysfunction. Components of the patient’s presentation are suggestive of critical hypothyroidism (myxedema coma) including alteration in mental status, QT-prolongation and hyponatremia as well as possible precipitant of pneumonia. However, despite elevated TSH, the patient’s free T4 level was within normal range. Also absent was hypoventilation (the patient was appropriately tachypneic for degree of hypoxia and with resultant respiratory alkalosis) or bradycardia/hypothermia.
Similarly, adrenal insufficiency is typically associated with hyperkalemia, whereas our patient had critical hypokalemia that was determined to be at least a contributory factor to her ventricular dysrhythmia. The etiology of the patient’s hypokalemia remained unexplained.
|Anaphylaxis||Exposure to allergen||Abrupt onset, facial swelling||Stridor, wheezing, hives|
|PE||Immobilization, malignancy, prior DVT/PE, surgery, OCP||Abrupt onset, pleuritic chest pain||Tachycardia, hypoxia||ECG (RV strain)
CT PA, D-dimer
LE US (DVT)
|Pneumonia||Exposure, tobacco use||Fever, productive cough||Focal rales||CXR
|Pneumothorax||Trauma, thin male||Abrupt onset, chest pain||Decreased BS, subQ emphysema, JVD and tracheal deviation if tension||CXR
|Fluid overload||Dietary indiscretion, medication non-adherence||Orthopnea, PND||JVD, S3/S4, peripheral edema||CXR
|COPD/Asthma||Tobacco use, personal/family history||Progressive||Retractions, accessory muscle use, wheezing||CXR
US (distinguish from fluid overload)
|Malignancy||Tobacco use, weight loss||Hemoptysis||CXR
The format of this article is atypical for the structure and concept of the website – but it’s always been about learning. Here is a simplified guide to ECG interpretation with a focus on the aspects I find more challenging to understand or recall.
|Distribution||Coronary Artery||Leads||Reciprocal Changes|
|1. Inferior||RCA, PDA||II, III, aVF||Anterior, Lateral|
|2. Lateral||LCx||I, aVL, V5, V6||Inferior|
|4. Posterior||RCA||Posterior||Anterior (esp. V1)|
70M with a history of dementia presenting with 3 days of fatigue. The patient was unable to provide detailed history, however family members reported worsening fatigue with the patient requiring assistance with ambulation for several days. The patient was referred from an outside clinic after point-of-care hemoglobin of 6.7. No reported history of anemia, and no history suggestive of obvious external bleeding.
Vital signs stable, tachycardia and tachypnea noted with minimal exertion but saturating well on ambient air and in no acute distress. Examination notable for conjunctival pallor without scleral icterus, systolic flow murmur, brown stool guaiac negative.
CBC with hemoglobin of 7.5 , MCV 80.3 , RDW 22.4 , no leukocytosis and normal platelets. Also noted was an alkaline phosphatase of 828 , normal total and direct bilirubin, and undetectable serum troponin. Chest x-ray showed a possible pleural-based mass.
The patient was transfused two units of PRBC’s and admitted for further evaluation. CT chest/abdomen/pelvis revealed sternal and rib-based pleural soft-tissue mass, prostate mass, pelvic and retroperitoneal lymphadenopathy as well as extensive bony metastatic disease consistent with primary prostate cancer with diffused metastasis. Serum PSA was 2,087 . Iron studies suggested anemia of chronic disease. Reticulocytes were not obtained but may have suggested inadequate production index given extensive bony metastases and possible associated myelosuppression. The patient was symptomatically improved after transfusion and discharged with outpatient follow-up for discussions regarding possible biopsy and treatment.
34 year-old male brought in by ambulance s/p assault. Field GCS reportedly 7, in trauma bay assessed as E2-V4-M6. Witnessed seizure in CT scanner, resolved with lorazepam. Intubated for airway protection, underwent external ventricular drain placement and transferred to surgical ICU.
Initial imaging revealed bifrontal subdural hematomas and right temporal hemorrhagic contusion with generalized edema. Repeat imaging one hour later showed interval development of large extra-axial hemorrhage overlying the right occipital and parietal lobes (2.2cm), representing subdural or epidural hematoma.
The patient’s ICU course was complicated by continued seizures and refractory elevation in intracranial pressure. A pentobarbital infusion was started and titrated to adequate burst suppression and hyperosmolar therapy with both mannitol and hypertonic saline continued. Additional imaging revealed stable hemorrhage but continued diffuse cerebral edema evidenced by sulcal effacement.
On hospital day 5, examination revealed bilateral fixed and dilated pupils. Imaging revealed effacement of basilar cisterns, pre-pontine cistern, and cisterna magna suggestive of impending/ongoing transtentorial and tonsillar herniation. Pentobarbital was weaned and conventional cerebral angiography as well as cerebral perfusion studies were consistent with brain death.
59F with a reported history of congestive heart failure, presenting with intermittent chest discomfort for three days.
She characterized this discomfort as “heartburn”, describing a mid-epigastric burning sensation radiating up her neck, not associated with exertion, lasting 1-2 hours and resolving with antacids. The patient has poor exercise tolerance at baseline and for the past several years has been able to ambulate only short distances around her home, and states that these symptoms have been worsening in the past week. She denies chest pain on exertion, orthopnea or paroxysmal nocturnal dyspnea. She states that she was diagnosed with congestive heart failure five years ago, but was never prescribed medications.
On further questioning, the patient reports several weeks of mouth and lip pain which has limited oral intake, though no dysphagia to solids or liquids. She otherwise denies fevers/chills, abdominal pain, nausea/vomiting, cough, changes in urinary or bowel habits.
In the emergency department, the patient was noted to have an elevated serum troponin, though ECG showed no changes of acute ischemia/infarction.
|Gen:||Morbidly obese female, lying in bed, in no acute respiratory distress, speaking in complete sentences.|
|HEENT:||Dry, cracked lips, slightly erythematous, otherwise moist mucous membranes, poor dentition. Mild scleral icterus. No cervical lymphadenopathy.|
|CV:||Rapid rate, regular rhythm, normal S1/S2, II/VI systolic ejection murmur at LUSB, no radiation appreciated. No jugular venous distension.|
|Lungs:||Clear to auscultation in posterior lung fields bilaterally, no crackles appreciated.|
|Chest:||Well-circumscribed erythematous patch in folds beneath left breast, no underlying fluctuance, no significant tenderness to palpation. On contralateral breast, some hyperpigmentation but no erythema.|
|Abdomen:||Obese, non-tender, non-distended. Patch of erythema below pannus, mildly tender to palpation.|
|Ext:||Bilateral lower extremities with marked edema and overlying scaly plaques, some slightly ulcerated weeping serous fluid. Peripheral pulses are difficult to palpate, capillary refill difficult to assess.|
CT Pulmonary Angiography:
No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax.
CT Abdomen/Pelvis non-contrast:
No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis.
CT Lower Extremity non-contrast:
Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening.
There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities.
Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance.
The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified.
Despite the patient’s reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patient’s significant lower extremity edema was more suggestive of chronic venous stasis.
One notable laboratory abnormality that was explored was her elevated anion gap metabolic acidosis. Studies submitted included serum lactate, salicylates, osmolarity, CK, and urinalysis for ketonuria. This evaluation was notable for an elevated serum lactate of 13.2mmol/L and an arterial blood gas that showed adequate respiratory compensation (and no A-a gradient). Given the patient’s modest leukocytosis (with neutrophil predominance), and tachycardia, the concern for sepsis was increased though the source remained unclear. Prominent possibilities included a skin and soft-tissue infection vs. less likely intra-abdominal source though the patient’s physical examination was not suggestive of a process that would produce such a substantial lactic acidosis. Blood cultures were drawn and the patient was started on empiric antibiotics for the suspected sources. In addition, the patient was cautiously volume resuscitated given her reported history of CHF while pending a transthoracic echocardiogram to evaluate cardiac function. Additional imaging including CT abdomen/pelvis and lower extremities was obtained (though without contrast due to the patient’s recent exposure), and no obvious source was identified.
Over the next two days, the patient’s serum lactate downtrended to normal range, as did the serum troponin. A transthoracic echocardiogram showed an LVEF >70% with mild concentric hypertrophy and diastolic dysfunction. Blood and urine cultures were without growth.
Additional issues managed during the hospitalization included elevated serum transaminases (AST > ALT), conjugated hyperbilirubinemia and evidence of decreased hepatic synthetic function with hypoalbuminemia and elevated INR. Given the patient’s history of EtOH use, as well as other corroborating findings including macrocytic anemia, hypomagnesemia, folate and B12 deficiency, this was attributed to alcoholic hepatitis (discriminant function <32). Infectious hepatitis serologies were negative. The patient was started on nutritional supplements. Finally, the patient persistently complained of lip and oral mucosal pain. Examination was without discrete lesions but some mucosal redness was identified. Despite poor dentition, there was no evidence of abscess and HSV/HIV testing was negative. This was thought to be stomatitis caused by her identified nutritional deficiencies.
64F with a history of CAD, MI, CHF, CLL and rheumatoid arthritis who presented to the emergency department after transfer from a rehabilitation facility for respiratory distress. The patient reported several days of progressive shortness of breath with dyspnea on exertion. She also noted some associated orthopnea and lower extremity edema. The patient was recently hospitalized for similar symptoms and was diagnosed with CHF at the time. At the rehab facility, the patient became hypoxemic and hypertensive, reporting shortness of breath and chest pain prior to presentation.
The patient was initially managed with BiPAP and nitroglycerin continuous infusion, but was then stable on supplemental O2 via nasal cannula and was transitioned to long-acting nitrates and anti-hypertensives. The patient’s hypoxemic respiratory failure was initially attributed to acute exacerbation of left-ventricular heart failure, and the patient was managed with spot diuresis. However, there was no symptomatic improvement and the patient became hypernatremic so diuresis was held as alternative diagnoses were explored.
A transthoracic echocardiogram showed preserved LVEF (50-55%), but some diastolic dysfunction and elevated PAP/RAP. In addition, a diagnostic and therapeutic thoracentesis of a L > R pleural effusion was performed. Pleural fluid studies were suggestive of a transudative process, though with some abnormal characteristics (including lymphocyte predominance, as well as presence of signet cells).
Rheumatology and pulmonology services were consulted for input and recommendations for further evaluation were appreciated. Per rheumatology, the patient’s diagnosis of rheumatoid arthritis may not be consistent with her presentation or prior serologic studies. Her pleural fluid analysis was also not consistent with rheumatoid disease. According to pulmonary consult, the patient’s hypoxemia remains most consistent with left ventricular dysfunction though primary pulmonary processes cannot be excluded (and would warrant further evaluation with imaging and pulmonary function testing).
|Gen:||Elderly female, alert and oriented to self and place, responding appropriately to questions.|
|HEENT:||Mucous membranes moist, sclera anicteric, no cervical lymphadenopathy.|
|CV:||Regular rate and rhythm, normal S1/S2, no additional heart sounds. III/VI mid-systolic murmur heard best at LLSB with diastolic component, no radiation appreciated. Non-displaced PMI. JVP measured to 14cm.|
|Lungs:||Decreased breath sounds in left lung field to inferior 2/3 with crackles above, on right crackles to inferior 1/2 of lung fields posteriorly. Dullness to percussion of inferior left lung field posteriorly.|
|Abdomen:||Soft, non-tender, non-distended, no hepatosplenomegaly, no appreciable fluid wave.||Ext:||Bilateral lower extremities with 2+ pitting edema to knees, some hyperpigmentation to right lower extremity.|
CT Chest (High-Resolution):
64F with history of CAD (prior MI), CHF, hypertension, CLL, hypothyroidism presented from a SNF with progressive shortness of breath, orthopnea and LE swelling, found to have bilateral (L>R) pleural effusion now s/p thoracentesis with transudative fluid.
#Acute hypoxic respiratory failure: Large pleural effusions, s/p thoracentesis with pleural fluid suggestive of transudative process. Most likely secondary to left ventricular diastolic dysfunction. Improved after thoracentesis and diuresis. High-resolution CT chest performed without evidence of autoimmune-related pulmonary fibrosis or ILD (though persistent pleural effusions, pulmonary vascular congestion).
#Pleural fluid signet cells: Identified on cytology, potentially related to history of untreated CLL or alternative primary malignancy.
#Left ventricular diastolic dysfunction, decompensated: Associated with pleural effusions and hypoxemic respiratory failure. Management with diuresis.
#Pulmonary Hypertension: Severe, noted on transthoracic echocardiography, may be secondary to hypoxemia associated with pleural effusions, consider repeat imaging once euvolemic or right-heart catheterization.
#Microscopic Hematuria: No evidence of infection, no symptoms suggestive of nephrolithiasis. No casts identified or significant proteinuria. Plan for renal ultrasound.
#Rheumatoid Arthritis: History of rheumatoid arthritis, on prednisone and hydroxychloroquine. Imaging without evidence of inflammatory arthropathy, RF elevated but CCP negative. Per rheumatology, the patient’s symptoms are not consistent with RA, continuing home medications while evaluation is ongoing. Pleural effusions unlikely associated with RA as transudative, and without monocyte predominance or low glucose.
Pleural effusions can be easily identified on chest radiography, physical examination findings include dullness to percussion, decreased tactile fremitus and decreased (or absent) breath sounds.
Notified by nursing of abnormal vital signs, SpO2 91%. Briefly, this patient is a 52 year-old G1P1 with no prior medical history who is post-operative day three status post total abdominal hysterectomy, bilateral salpingoophorectomy as well as tumor debulking and staging for suspected primary ovarian adenocarcinoma based on peritoneal fluid cyctology.
On evaluation, the patient denied shortness of breath, chest pain, pleuritic chest pain, cough/hemoptysis, or calf/thigh pain. She states that she had been ambulating around the ward prior to having her vital signs assessed.
|Gen:||No acute distress, speaking in full sentences.|
|HEENT:||No jugular venous distension.|
|CV:||RRR, normal S1/S2, no prominent P2, no additional heart sounds.|
|Lungs:||Decreased breath sounds at inferior 1/3 posterior lung fields bilaterally, faint crackles above, no wheezing. Dullness to percussion in inferior lung fields.|
|Ext:||Warm, well-perfused. Sequential compression devices on bilateral lower extremities, removed revealing trace pitting edema symmetric bilaterally, no tenderness to palpation of posterior leg, no pain with passive dorsiflexion.|
52yo G1P1 with likely primary ovarian adenocarcinoma with extensive peritoneal involvement, complicated by malignant ascites and pleural effusions with hypoxemia. The primary concern in this post-operative patient with a history of malignancy is venous thromboembolism, particularly pulmonary embolism. Aside from hypoxemia, this patient had no symptoms suggestive of pulmonary embolism (denied dyspnea, chest pain, cough, or lower extremity pain). Her examination had some signs infrequently associated with pulmonary embolism which were otherwise adequately explained by known bilateral pleural effusions (including decreased breath sounds, rales, and tachypnea), she was not tachycardic, had no evidence of jugular venous distension, nor a prominent P2. In addition, she was receiving appropriate VTE prophylaxis (both pharmacological and mechanical). The application of the Modified Wells clinical decision rule suggests low likelihood of pulmonary embolism (with 2.5 points assigned for recent surgery and history of malignancy). The patient had a recent CT chest without evidence of pulmonary embolism, and given that an elevated D-dimer was virtually assured which would have necessitated repeat imaging (and the associated risks of radiation exposure and contrast injury), the episode was ascribed to ventilation/perfusion mismatch secondary to large pleural effusions. Hypoxemia resolved after several minutes at rest and no further testing was performed.
|Tachycardia||Pleurtic chest pain|
|Decreased breath sounds||Orthopnea|
|Prominent P2||Calf/thigh pain or swelling|
|Clinical symptoms of DVT (leg swelling, tenderness to palpation)||3.0|
|Pulmonary embolism most likely diagnosis||3.0|
|Tachycardia (HR >100)||1.5|
|Immobilization >3d, surgery in prior 4 weeks||1.5|
48F with a history of SLE presenting with two weeks of fevers and joint pain. The patient reports progressive development of these symptoms associated with malaise and muscle aches. She also reports two days of cough productive of yellow sputum, but denies chest pain, shortness of breath or hemoptysis. She states that these symptoms are comparable to prior lupus flares but have persisted longer than usual. She has not travelled or been hospitalized recently and has no sick contacts.
|VS:||T||39.4||HR||138||RR||19||BP||97/61||O2||98% 2L NC|
|Gen:||Alert, responsive and in no acute distress.|
|HEENT:||PERRL, dry mucous membranes, no oropharyngeal lesions or erythema, TM intact bilaterally, no cervical lymphadenopathy, neck supple.|
|CV:||Tachycardia, regular rhythm without additional heart sounds.|
|Lungs:||Clear to auscultation bilaterally.|
|Abd:||+BS, soft, non-tender, non-distended, no rebound/guarding.|
|Ext:||No peripheral edema, extremities warm and well-perfused, diffuse tenderness to palpation and resisted range of motion of joints with particular involvement of bilateral shoulders, elbows, knees and ankles. No effusion noted, no erythema or warmth.|
|Neuro:||Alert, oriented to self, location and time. PERRL, EOMI, facial sensation intact, facial muscles symmetric, palate rises symmetrically, tongue protrudes midline without fasciculation, peripheral sensation and motor strength grossly intact with normal gait.|
48F with a history of SLE presenting with fever and polyarticular arthralgia.
#SIRS: Fever and tachycardia in the setting of immunosuppression. The differential diagnosis includes pneumonia (bacterial, viral, less-likely fungal), which would be community-acquired. Association with polyarticular arthralgia suggests symptoms may represent lupus flare given no leukocytosis and elevated CRP.
#Hypocalcemia: Asymptomatic, likely due to hypoalbuminemia and hypomagnesemia. Improved after IV fluids and correction of hypokalemia, hypomagnesemia.
The patient was admitted and completed a 7-day course of ceftriaxone and azithromycin. Rheumatology was consulted for management of lupus flare, which included resuming home medications and a prednisone taper upon discharge.
The patient was admitted ten days later, presenting with fevers, productive cough and pleuritic chest pain. Found to have a left lower lobe sub-segmental pulmonary embolus and antiphospholipid syndrome. She was also treated empirically for healthcare-associated pneumonia with cefepime and vancomycin given fever and productive cough though there were no imaging findings suggestive of consolidation and sputum cultures were negative.
It is important to differentiate whether fever in a patient with SLE is due to disease activity (flare) or active infection.
Routine laboratory studies are common in the intensive care unit; abnormalities are even more common. Typically these studies include a chemistry panel (Chem 10). The differential diagnoses of the most frequent and clinically relevant electrolyte abnormalities are detailed below.