1. ACUTE BLOOD LOSS ANEMIA
Q1: What is the definition of Acute Blood Loss Anemia?
A1: Acute Blood Loss Anemia refers to anemia resulting from acute bleeding or hemorrhage, irrespective of the source, even if anticipated.
Q2: What hemoglobin level is used to measure anemia in men?
A2: For men, anemia is diagnosed when the hemoglobin level is less than 13.0 gm/dl.
Q3: What hemoglobin level is used to measure anemia in non-pregnant women?
A3: For non-pregnant women, anemia is diagnosed when the hemoglobin level is less than 12.0 gm/dl.
Q4: What hemoglobin level is used to measure anemia during pregnancy?
A4: During pregnancy, anemia is diagnosed when the hemoglobin level is less than 11.0 gm/dl.
Q5: What is the general rule of thumb comparing hemoglobin to hematocrit?
A5: Generally, one gm/dl of hemoglobin is equivalent to a hematocrit of 3%.
Q6: How much is a transfusion of one unit of blood expected to increase the hemoglobin level?
A6: A transfusion of one unit of blood is expected to increase the hemoglobin level by approximately 1 gm/dl.
Q7: What drop in hemoglobin or hematocrit suggests a clinically significant decrease?
A7: A clinically significant decrease is suggested by a drop in hemoglobin of 2.0 gm/dl or more, or a drop in hematocrit of 5% or more.
Q8: How does a patient's baseline affect the significance of a hemoglobin decrease?
A8: A smaller decrease in hemoglobin is more significant when the baseline level is lower.
Q9: Is a blood transfusion required to diagnose acute blood loss anemia?
A9: A transfusion is not required for diagnosis; monitoring serial hemoglobin levels is sufficient.
Q10: What clinical developments suggest a drop in hemoglobin significant enough to elicit concern?
A10: Concerning clinical developments include the need for transfusion, the onset of previously absent anemia symptoms, and intensive serial monitoring of hemoglobin.
2. ACUTE KIDNEY INJURY (AKI)
Q1: What is the definition of Acute Kidney Injury (AKI)?
A1: AKI is characterized by a sudden reduction in kidney function, typically occurring within hours or days.
Q2: What is the most common pre-renal cause of AKI?
A2: Dehydration is the most prevalent pre-renal cause of AKI.
Q3: What are examples of renal causes of AKI?
A3: Renal causes include acute tubular necrosis (ATN), acute papillary necrosis, and glomerulonephritis.
Q4: What is a post-renal cause of AKI?
A4: A post-renal cause involves the obstruction of ureters or the bladder.
Q5: What consensus-based criteria are currently used to define AKI?
A5: The current consensus-based criteria for AKI are defined by the National Kidney Foundation (NKF) KDIGO conference.
Q6: According to KDIGO, what relative increase in creatinine defines AKI?
A6: AKI is defined by a creatinine level increase of 1.5 times the baseline (historical or measured), known or presumed to have occurred within the preceding 7 days.
Q7: According to KDIGO, what absolute increase in creatinine defines AKI?
A7: AKI is defined by an absolute increase in creatinine of 0.3 mg/dl or more from baseline within 48 hours.
Q8: According to KDIGO, what urine output parameter defines AKI?
A8: AKI is defined by a urine output of less than 0.5 ml/kg/hr for 6 hours.
Q9: Do KDIGO criteria apply only to adults?
A9: These criteria are applicable to both adult and pediatric patients.
Q10: How does KDIGO advise diagnosing AKI when baseline creatinine is unknown?
A10: KDIGO suggests that the lowest serum creatinine recorded during hospitalization is typically equal to or greater than the baseline and should be utilized for diagnosing and staging AKI.
3. ACUTE TUBULAR NECROSIS (ATN)
Q1: What is Acute Tubular Necrosis (ATN)?
A1: ATN is a functional abnormality of the renal tubules resulting from toxic or ischemic injury, which, if severe, can progress to necrosis and sloughing of renal tubular cells.
Q2: How long does the duration of renal tubular dysfunction in ATN range?
A2: The duration of dysfunction varies from transient (lasting more than 72 hours) to the prolonged, classic presentation of pathological tubular necrosis.
Q3: What distinction differentiates prerenal AKI from ATN?
A3: The distinction is based on the clinical context leading to AKI and the rapidity of the creatinine response to intravenous fluid resuscitation.
Q4: Which IV administration always causes ATN?
A4: Intravenous contrast consistently induces ATN.
Q5: What are some common medications that cause ATN?
A5: Medications commonly associated with ATN include acetaminophen, NSAIDs, cyclosporine, cisplatin, acyclovir, tetracycline, and aminoglycosides.
Q6: How long is renal function expected to take to return to baseline in ATN after hydration?
A6: Renal function is expected to require more than 72 hours to return towards baseline following effective intravenous fluid resuscitation.
Q7: What is the diagnostic urine sodium concentration for ATN?
A7: The typical diagnostic urine sodium concentration is greater than 40 meq/L.
Q8: What is the diagnostic Fractional Excretion of Sodium (FENa) for ATN?
A8: The FENa is usually greater than 2%, though occasionally it can be less than 2%.
Q9: What might the urine sediment show in ATN?
A9: The urine sediment may reveal muddy brown granular casts.
Q10: Why is a urinalysis used in evaluating ATN today?
A10: Currently, urinalysis is not used for primary diagnosis but rather to exclude other intrarenal conditions such as glomerulonephritis and acute interstitial nephritis.
4. BMI
Q1: What is required from a provider to code a BMI?
A1: A BMI cannot be coded without an associated, reportable diagnosis documented by a provider, such as obesity, overweight, OHS, malnutrition, anorexia, or underweight.
Q2: What BMI levels are considered Comorbidities or Complications (CCs)?
A2: A BMI of 40.0 or greater, and a BMI of less than 19.9, are classified as CCs.
Q3: Is Obesity Hypoventilation Syndrome (OHS) considered a CC?
A3: Yes, OHS is classified as a CC.
Q4: What is the former name for Obesity Hypoventilation Syndrome?
A4: OHS was previously known as Pickwickian syndrome.
Q5: How is Obesity Hypoventilation Syndrome defined?
A5: OHS is defined as the presence of awake hypoventilation associated with obesity (BMI > 30) that cannot be attributed to another condition, causing chronic hypercapnia and daytime somnolence with episodes of hypoxemia.
Q6: What BMI range indicates morbid obesity?
A6: A BMI of 40.0 or greater indicates morbid obesity.
Q7: What BMI range indicates severe obesity?
A7: A BMI between 35 and 39.9 indicates severe obesity.
Q8: What BMI range indicates standard obesity?
A8: A BMI between 30 and 39.9 indicates obesity.
Q9: What BMI range indicates a patient is overweight?
A9: A BMI between 25 and 29.9 indicates that a patient is overweight.
Q10: What BMI range indicates a patient is underweight or malnourished?
A10: A BMI of less than 18.5 indicates underweight or malnutrition.
5. CEREBRAL EDEMA
Q1: What is the definition of cerebral edema?
A1: Cerebral edema refers to swelling within the brain.
Q2: What are common causes of cerebral edema?
A2: Common causes include trauma, neoplasm, CVA, intracerebral hemorrhage, hypoxic brain injury, postsurgical complications, brain abscess, toxins, and extreme electrolyte abnormalities.
Q3: How is cerebral compression defined?
A3: Cerebral compression is characterized by pressure on the brain that typically causes displacement, often resulting in some degree of herniation, though not always.
Q4: What can cause cerebral compression?
A4: Common causes include cerebral edema, traumatic brain injury, any intracranial mass such as neoplasm, hemorrhage/hematoma, hydrocephalus, and brain abscess.
Q5: What is cerebral herniation?
A5: Cerebral herniation is the displacement of a portion of the brain across or through a fixed intracranial structure.
Q6: What structures might the brain herniate through?
A6: The brain may herniate through fixed intracranial structures such as the falx, tentorium, or foramen magnum.
Q7: Which imaging study is usually employed to diagnose cerebral edema?
A7: A brain CT scan is typically utilized for diagnosis.
Q8: What additional benefit does an MRI offer for diagnosing these conditions?
A8: An MRI clearly demonstrates edema or compression and can provide supplementary information.
Q9: How does cerebral edema manifest on an imaging study?
A9: Cerebral edema appears as one or more areas of decreased/low brain density on imaging, sometimes described as vasogenic.
Q10: What might imaging studies show in cases of cerebral compression or herniation?
A10: Imaging studies may reveal mass effect, midline shift, effacement of ventricles and/or cerebral sulci, a space-occupying lesion, or acute hydrocephalus.
6. CVA
Q1: How is a Cerebrovascular Accident (CVA) defined?
A1: A CVA is defined as a brain infarction or hemorrhage, typically associated with permanent or temporary neurological deficits.
Q2: Does a transient focal neurologic deficit count as a CVA?
A2: Yes, it includes transient focal neurological deficits that persist for longer than 24 hours.
Q3: What imaging findings act as a clinical indicator for a CVA?
A3: A positive MRI or CT scan showing acute infarction or hemorrhage serves as an indicator.
Q4: Can a CVA be diagnosed without positive imaging?
A4: Yes, a persistent focal neurological deficit lasting greater than 24 hours can indicate a CVA, irrespective of imaging results.
Q5: What is the best test to evaluate an acute CVA?
A5: An MRI without contrast, if available, is likely the optimal test for evaluating an acute CVA.
Q6: Why is a CT typically used acutely for a CVA?
A6: A CT scan is typically used acutely to exclude hemorrhage.
Q7: How long might it take for a non-hemorrhagic CVA to become visible on a CT?
A7: A non-hemorrhagic CVA may not be visible on a CT during the initial 24 hours, becoming evident only after several days.
Q8: What are two initial treatments for a CVA?
A8: Initial treatments include anti-platelet or anti-thrombotic therapy and frequent neurological assessments.
Q9: Under what circumstances is TPA (tissue plasminogen activator) used?
A9: TPA is utilized as a treatment in specific circumstances.
Q10: How do coding classifications differ between hemiplegia and monoplegia?
A10: Hemiplegia codes are classified as CCs, whereas monoplegia codes are neither CCs nor MCCs.
7. CKD
Q1: What is the GFR diagnostic criterion for Chronic Kidney Disease (CKD)?
A1: The diagnostic criteria for CKD include a decreased GFR of less than 60 ml/min, present for more than 3 months.
Q2: What alternative criteria besides GFR can diagnose CKD?
A2: Alternative criteria include objective measures of kidney damage, such as significant persistent albuminuria, urinary sediment abnormalities, electrolyte abnormalities, abnormalities on biopsy, structural abnormalities on imaging, or a history of kidney transplant.
Q3: How is the stable baseline GFR used in CKD?
A3: Five stages of CKD are identified based on the stable baseline GFR.
Q4: What GFR corresponds to Stage 1 CKD?
A4: A GFR of 90 ml/hr or greater corresponds to Stage 1 CKD.
Q5: What GFR corresponds to Stage 2 CKD?
A5: A GFR ranging from 60-89 ml/hr corresponds to Stage 2 CKD.
Q6: What GFR corresponds to Stage 3b CKD?
A6: A GFR ranging from 30-44 ml/hr corresponds to Stage 3b CKD.
Q7: What GFR corresponds to Stage 4 CKD?
A7: A GFR ranging from 15-29 ml/hr corresponds to Stage 4 CKD.
Q8: What defines End-Stage Renal Disease (ESRD)?
A8: ESRD is defined as a GFR of less than 15 ml/hr and dependence on dialysis.
Q9: Can a patient with a GFR >= 60 ml/min have CKD without other markers?
A9: No, a GFR of 60 ml/min or greater does not indicate CKD in the absence of other markers of kidney damage.
Q10: Which stages of CKD are considered Comorbidities or Complications (CCs)?
A10: CKD stages 4 and 5 are classified as CCs.
8. DIABETIC COMPLICATIONS - HHS, DKA
Q1: What characterizes Diabetic Hyperglycemia Hyperosmolar State (HHS)?
A1: HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis, typically accompanied by some alteration in consciousness.
Q2: What blood sugar level is required to diagnose HHS?
A2: The diagnostic criteria include a blood sugar greater than 250 mg/dl, but it is commonly above 600 mg/dl.
Q3: What osmolarity level is required to diagnose HHS?
A3: The diagnostic criteria include an osmolarity greater than 320 mmol/L.
Q4: What characterizes Diabetic Ketoacidosis (DKA)?
A4: DKA is characterized by hyperglycemia, acidosis, elevated serum ketones, and dehydration.
Q5: What blood sugar level is required to diagnose DKA?
A5: The diagnostic criteria require a blood sugar greater than 250 mg/dl.
Q6: What pH level indicates acidosis for a DKA diagnosis?
A6: Acidosis, with a pH less than 7.30, is required.
Q7: What bicarbonate level is required for a DKA diagnosis?
A7: A bicarbonate level less than 18 mEq/L is required.
Q8: What type of ketones must be elevated to diagnose DKA?
A8: There must be a marked elevation of serum ketones, not urinary ketones.
Q9: What initial medication is used to treat HHS and DKA?
A9: Treatment typically involves insulin, usually initiated intravenously.
Q10: Are Diabetic Complications like HHS and DKA considered MCCs?
A10: Yes, diabetic complications such as HHS and DKA are classified as MCCs.
9. ENCEPHALOPATHY/AMS
Q1: How does the NIH describe encephalopathy?
A1: The NIH describes encephalopathy as any diffuse brain disease that alters brain function or structure.
Q2: How can encephalopathy be further classified?
A2: Encephalopathy can be further categorized as acute (functional) or chronic (structural).
Q3: What causes acute encephalopathy?
A3: It is primarily caused by a systemic underlying condition.
Q4: Does acute encephalopathy cause structural changes?
A4: No, structural changes do not occur, and the condition is reversible once the underlying cause is addressed.
Q5: What would a CT or MRI scan show in acute encephalopathy?
A5: A CT/MRI is expected to be unremarkable, as the brain abnormality is functional rather than structural.
Q6: What is the purpose of an EEG in diagnosing acute encephalopathy?
A6: An EEG may show diffuse slowing or low amplitude and can help exclude subclinical seizures.
Q7: What are the causes of metabolic encephalopathy?
A7: Causes include fever, dehydration, electrolyte imbalance, acidosis, hypoxia, infection, and organ failure.
Q8: What causes hepatic encephalopathy?
A8: It is caused by elevated blood ammonia levels and describes a spectrum of neurological impairment in patients with severe end-stage liver disease.
Q9: What marks hypertensive encephalopathy?
A9: It is characterized by headache, obtundation, confusion, or stupor, which may or may not be accompanied by convulsions.
Q10: Who is commonly affected by hypoxic ischemic encephalopathy?
A10: This condition applies to neonates and is frequently observed in premature infants.
10. HEART FAILURE
Q1: What physical exam findings can indicate a heart failure exacerbation?
A1: Physical examination findings may include rales and/or increasing edema.
Q2: What might a chest x-ray show in a patient with heart failure?
A2: A chest x-ray may reveal pulmonary edema/congestion, increasing or new pleural effusion, and cardiomegaly.
Q3: What BNP level supports a diagnosis of heart failure?
A3: A BNP level greater than 500 supports the diagnosis.
Q4: What NT-pro-BNP level indicates heart failure in a patient older than 75 without renal impairment?
A4: An NT-pro-BNP level greater than 1,800 indicates heart failure for patients over 75 years of age.
Q5: What defines Systolic Heart Failure?
A5: Systolic Heart Failure is defined as heart failure with a left ventricular ejection fraction of less than 50%.
Q6: What defines Diastolic Heart Failure?
A6: Diastolic Heart Failure is defined as heart failure with a left ventricular ejection fraction of 50% or greater.
Q7: What is the most common cause of Systolic Heart Failure?
A7: The most common cause is ischemic heart disease, such as CAD.
Q8: What are the most common causes of Diastolic Heart Failure?
A8: The most common causes are hypertension and/or ESRD.
Q9: Name two diuretics used in the treatment of heart failure.
A9: Diuretics employed include Lasix (furosemide) and Bumex (bumetanide).
Q10: How are acute forms of heart failure classified for coding?
A10: All acute and acute-on-chronic forms of heart failure are classified as MCCs.
11. HTN CRISIS AND EMERGENCY
Q1: What is a hypertensive crisis?
A1: Hypertensive crisis is a non-specific, general term for a severe elevation of blood pressure, encompassing both hypertensive urgency and emergency.
Q2: What blood pressure values usually define a severe elevation?
A2: Severe elevation is typically defined as a systolic BP greater than 180 mmHg or a diastolic BP greater than 120 mmHg.
Q3: How is hypertensive emergency defined?
A3: It is defined as a severe elevation of blood pressure representing a serious, potentially life-threatening condition that necessitates aggressive intervention to immediately lower blood pressure, with evidence of end-organ involvement.
Q4: What differentiates hypertensive urgency from an emergency?
A4: Hypertensive urgency is characterized by severe blood pressure elevation without end-organ involvement.
Q5: What cardiovascular end-organ involvement can occur in a hypertensive emergency?
A5: It may include heart failure, unstable angina, or myocardial infarction.
Q6: What neurologic end-organ involvement can occur in a hypertensive emergency?
A6: It may include hypertensive encephalopathy, seizure, stroke, or brain hemorrhage.
Q7: How is hypertensive urgency typically treated?
A7: It is treated with a gradual reduction of blood pressure over hours or days using typical oral antihypertensives.
Q8: Should blood pressure be rapidly reduced in a hypertensive urgency?
A8: No, aggressive immediate reduction is not recommended for hypertensive urgency.
Q9: How is a hypertensive emergency treated?
A9: It requires an immediate, urgent reduction using intravenous antihypertensives.
Q10: What are some examples of IV antihypertensives used for emergencies?
A10: Examples include nitroprusside, nitroglycerin, labetalol, nicardipine, esmolol, and hydralazine.
12. MALNUTRITION
Q1: What are the three clinical contexts for malnutrition defined by ASPEN criteria?
A1: The contexts are acute illness or injury, chronic illness, and social/environmental circumstances.
Q2: How many clinical characteristics are required to meet ASPEN criteria for malnutrition?
A2: The diagnosis of malnutrition is based on the presence of at least two of six specified characteristics.
Q3: What constitutes an acute illness according to ASPEN?
A3: An acute illness has a duration of less than 3 months, exemplified by GI surgery, multi-system trauma, intubation, prolonged vomiting, or limited oral food intake.
Q4: What is the weight loss criteria for severe malnutrition in an acute context over 1 month?
A4: The criterion is a weight loss of greater than 5% in 1 month.
Q5: What is the energy intake criteria for severe malnutrition in a chronic illness context?
A5: The criterion is an energy intake of less than 75% of the estimated energy requirement for more than 1 month.
Q6: How is muscle mass loss categorized in non-severe malnutrition under ASPEN?
A6: Muscle mass loss is categorized as mild.
Q7: How does GLIM define malnutrition?
A7: GLIM defines malnutrition as a combination of reduced food intake or assimilation and varying degrees of acute or chronic inflammation, leading to altered body composition and diminished biological function.
Q8: What is the non-severe GLIM criteria for low BMI in a patient aged 70 or older?
A8: The non-severe criterion is a BMI of less than 22.
Q9: What is the severe GLIM criteria for unintended weight loss over a period > 6 months?
A9: The severe criterion is a weight loss of greater than 20%.
Q10: How is severe malnutrition coded?
A10: Severe malnutrition is classified as an MCC.
13. MYOCARDIAL INFARCTION
Q1: How is a myocardial infarction (MI) defined?
A1: MI is defined as acute myocardial injury accompanied by clinical evidence of myocardial ischemia.
Q2: What characterizes a Type 1 MI?
A2: Type 1 is characterized by coronary artery disease with plaque rupture and coronary thrombosis.
Q3: What characterizes a Type 2 MI?
A3: Type 2 is characterized by an imbalance between oxygen supply and myocardial demand without thrombosis.
Q4: What distinguishes NSTEMI from STEMI infarctions on an EKG?
A4: NSTEMI is identified by elevated troponin levels with only minor non-specific ST/T-wave changes or a normal EKG, and it does not produce Q waves or ST elevation.
Q5: What are some common causes of a Type 2 MI?
A5: Common causes include coronary artery spasm, embolism, or dissection, sustained tachy- or brady-arrhythmia, severe anemia, hypotension, shock, or severe hypertension.
Q6: What is required for the diagnostic criteria of a Type 1 MI regarding lab values?
A6: It requires acute myocardial injury, indicated by an elevated troponin level above the 99th percentile.
Q7: What EKG changes support the diagnosis of a Type 1 MI?
A7: New ischemic EKG changes such as ST elevation or depression, T-wave inversion, or hyperacute T-waves support the diagnosis.
Q8: What imaging evidence supports a Type 2 MI?
A8: Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality in a pattern consistent with an ischemic etiology supports the diagnosis.
Q9: What are common symptoms of acute myocardial ischemia?
A9: Symptoms include chest pressure or pain, neck, jaw, shoulder or arm pain, shortness of breath, nausea, vomiting, or diaphoresis.
Q10: Which biomarker is preferred over troponin T for evaluation of myocardial injury?
A10: Troponin I is preferred over troponin T.
14. PANCREATITIS
Q1: What is the definition of pancreatitis?
A1: Pancreatitis is the inflammation of the pancreas, not typically associated with infection.
Q2: How many diagnostic findings does the American College of Gastroenterology recommend to indicate acute pancreatitis?
A2: The American College of Gastroenterology recommends two or more of three specific findings.
Q3: What type of abdominal pain is consistent with pancreatitis?
A3: The pain is typically severe, constant, steady, and boring in nature.
Q4: Is the pain of pancreatitis dull or colicky?
A4: No, it is not dull, colicky, or of varying intensity.
Q5: Where is the pain typically located in pancreatitis?
A5: The pain is usually located in the epigastric region, left upper quadrant (LUQ), left flank, or back.
Q6: What is the diagnostic threshold for lipase and/or amylase?
A6: The levels must be greater than 3 times the upper limit of normal.
Q7: Why is an amylase or lipase elevation of less than 3 times the upper limit considered non-specific?
A7: This elevation is considered non-specific because it can be caused by numerous conditions, such as gastroenteritis, cholecystitis, bowel obstruction, and peptic ulcer.
Q8: What imaging studies can show characteristic findings of acute pancreatitis?
A8: Ultrasound, CT, and MRI can all demonstrate characteristic findings.
Q9: How is acute pancreatitis classified for coding?
A9: Acute pancreatitis is classified as an MCC.
Q10: How is chronic pancreatitis classified for coding?
A10: Chronic pancreatitis is classified as a CC.
15. PANCYTOPENIA
Q1: What is pancytopenia?
A1: Pancytopenia is a simultaneous deficiency in all three blood cell lineages: red blood cells, platelets, and neutrophils.
Q2: What is the clinical significance of anemia in pancytopenia?
A2: The clinical significance is decreased tissue oxygen supply.
Q3: What is the clinical significance of thrombocytopenia in pancytopenia?
A3: The clinical significance is an increased risk of bleeding.
Q4: What is the clinical significance of neutropenia in pancytopenia?
A4: The clinical significance is susceptibility to infection.
Q5: What are some possible causes of pancytopenia?
A5: Causes include malignancy, chemotherapy, other medications, myelodysplasia, aplastic anemia, radiation, and splenomegaly.
Q6: What absolute neutrophil count defines neutropenia?
A6: Neutropenia is defined by an absolute neutrophil count of less than 1.8k.
Q7: What platelet count defines thrombocytopenia?
A7: Thrombocytopenia is defined by a platelet count of less than 150k.
Q8: What hemoglobin level defines anemia in men for pancytopenia criteria?
A8: Anemia is defined as a hemoglobin level less than 13.0 gm/dL in men.
Q9: What hemoglobin level defines anemia in non-pregnant women for pancytopenia criteria?
A9: Anemia is defined as a hemoglobin level less than 12.0 gm/dL in women.
Q10: Why is it crucial to identify chemotherapy or other drugs as the cause of pancytopenia?
A10: It is crucial because these codes are classified as MCCs, whereas unspecified pancytopenia is only a CC.
16. PNEUMONIA
Q1: What type of diagnosis is pneumonia primarily?
A1: Pneumonia is primarily a clinical diagnosis, not culture-based, and is usually confirmed by chest x-ray.
Q2: What physical exam findings can suggest pneumonia?
A2: Findings may include rales, rhonchi, bronchial breath sounds, dullness to percussion, pleural rub, and chest wall splitting.
Q3: What happens to the WBC count in pneumonia?
A3: The WBC count may be low, normal, or elevated.
Q4: What does a chest x-ray usually show for pneumonia?
A4: It typically shows consolidation, infiltrate, or interstitial changes.
Q5: Why might consolidation or infiltrates be delayed on a chest x-ray?
A5: Their appearance may be delayed by one or two days, particularly if the patient is initially dehydrated.
Q6: Can pneumonia be diagnosed if a chest x-ray is negative?
A6: Yes, pneumonia can be diagnosed based solely on clinical grounds, even when imaging is negative.
Q7: What should a provider do if diagnosing pneumonia with negative radiographic findings?
A7: The provider should make a specific reference to the clinical basis of the diagnosis, also noting the absence of radiographic findings.
Q8: What antibiotic is used to treat Pseudomonas or Hemophilus pneumonia?
A8: Ciprofloxacin is used to treat these types.
Q9: Which antibiotics are effective against MRSA pneumonia?
A9: Zyvox (Linezolid) is effective against MRSA.
Q10: What is considered a classic location for an infiltrate in aspiration pneumonia?
A10: A Right Lower Lobe (RLL) infiltrate on a chest x-ray is considered a classic location.
17. RESPIRATORY FAILURE
Q1: What room air ABG finding indicates acute hypoxic respiratory failure?
A1: A pO2 of less than 60 mmHg on room air, measured by ABG, indicates acute hypoxic respiratory failure.
Q2: What room air pulse oximetry reading indicates acute hypoxic respiratory failure?
A2: An SpO2 of less than 91% on room air indicates acute hypoxic respiratory failure.
Q3: What P/F ratio indicates acute hypoxic respiratory failure?
A3: A P/F ratio of less than 300 on oxygen indicates acute hypoxic respiratory failure.
Q4: What pCO2 level defines acute hypercapnic respiratory failure?
A4: A pCO2 greater than 50 mmHg defines acute hypercapnic respiratory failure.
Q5: What pH level defines acute hypercapnic respiratory failure?
A5: A pH less than 7.35 defines acute hypercapnic respiratory failure.
Q6: How is the P/F ratio calculated?
A6: It is calculated by dividing the PaO2 by the FIO2.
Q7: When is the P/F ratio most useful?
A7: It is a powerful tool for identifying acute hypoxemic respiratory failure when supplemental oxygen is already being administered, and no room air ABG or SpO2 is available.
Q8: Why does a P/F ratio < 300 confirm hypoxemic respiratory failure?
A8: Because it is equivalent to a room air pO2 of less than 60 mmHg.
Q9: What room air pO2 equivalent does a P/F ratio of < 250 represent?
A9: It is equivalent to a pO2 on room air of 40-49, indicating severe respiratory failure.
Q10: If the SpO2 is 93%, what is the approximated pO2 used for a P/F ratio calculation?
A10: An SpO2 of 93% approximates a pO2 of 68 mm Hg.
18. RHABDOMYOLYSIS
Q1: What is rhabdomyolysis?
A1: Rhabdomyolysis is the necrosis of muscle tissue with the subsequent release of creatine kinase (CK) and myoglobin.
Q2: What is a severe complication of rhabdomyolysis?
A2: When severe, it commonly leads to AKI due to ATN.
Q3: What are some causes of rhabdomyolysis?
A3: Causes include prolonged pressure on muscle tissue, severe soft tissue trauma, extreme muscular exertion, adverse effects of medication, alcohol, illicit drugs, myopathy, viral infections, and sepsis.
Q4: What is the typical creatine kinase (CK) level at presentation for rhabdomyolysis?
A4: CK levels at presentation are usually 5 times the upper limit of normal, ranging from approximately 1,500 to over 100k units/L.
Q5: What is the normal reference range for CK?
A5: The normal reference range is approximately 22 to 198 (up to 300) units/L, varying by gender and the specific laboratory test used.
Q6: What other marker might be elevated in rhabdomyolysis besides CK?
A6: Myoglobin is often elevated in the urine and/or serum.
Q7: How often does muscle pain occur in cases of rhabdomyolysis?
A7: Muscle pain is observed in approximately 50% of cases.
Q8: What is the primary treatment for rhabdomyolysis to prevent ATN?
A8: Aggressive intravenous fluids are administered to prevent ATN.
Q9: How is non-traumatic or unspecified rhabdomyolysis coded?
A9: Non-traumatic or unspecified rhabdomyolysis is coded as a CC.
Q10: How is traumatic rhabdomyolysis coded?
A10: Traumatic rhabdomyolysis is classified as neither a CC nor an MCC.
19. SEPSIS-2
Q1: How does Sepsis-2 define sepsis?
A1: Sepsis is defined as SIRS due to an infection, whether suspected or confirmed.
Q2: What does SIRS stand for?
A2: SIRS stands for Systemic Inflammatory Response Syndrome.
Q3: Under Sepsis-2, what temperature thresholds meet the criteria?
A3: A temperature greater than 38C (>100.4 F) or less than 36 C (96.8 F) meets the criteria.
Q4: What heart rate variable indicates sepsis under Sepsis-2?
A4: A heart rate greater than 90/min meets the criteria.
Q5: What respiratory rate indicates tachypnea in the Sepsis-2 criteria?
A5: Tachypnea, with a respiratory rate greater than 20/min, meets the criteria.
Q6: What WBC values satisfy the inflammatory variable for leukocytosis?
A6: A WBC greater than 12K, a WBC less than 4K, or bands greater than 10% satisfy the variable.
Q7: What systolic blood pressure values indicate hemodynamic instability in Sepsis-2?
A7: A systolic blood pressure less than 90, a MAP less than 70, or a systolic blood pressure decrease greater than 40 indicates instability.
Q8: Which criteria very strongly support the diagnosis of sepsis?
A8: The temperature, WBC, lactate level, and persistent hypotension criteria very strongly support the diagnosis.
Q9: Why should tachypnea and tachycardia not be the only criteria used for diagnosing sepsis?
A9: Because tachypnea and tachycardia are very common in hospitalized patients for various reasons.
Q10: What ultimately determines the diagnosis of sepsis using these criteria?
A10: The diagnosis depends entirely on the physician's clinical interpretation of these criteria and their significance.
20. SEPSIS-3
Q1: How is organ dysfunction determined in Sepsis-3?
A1: Organ dysfunction is determined by a 2-point change from the baseline of the Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score.
Q2: How many organ systems are evaluated using the SOFA score?
A2: Six defined organ systems are evaluated.
Q3: What objective measurement evaluates the respiratory system in the SOFA score?
A3: The PaO2/FIO2 (P/F ratio) is utilized.
Q4: What objective measurement evaluates coagulation in the SOFA score?
A4: The platelet count is utilized.
Q5: What objective measurement evaluates the liver in the SOFA score?
A5: The bilirubin level in mg/dL is utilized.
Q6: What objective measurement evaluates cardiovascular function in the SOFA score?
A6: The Mean Arterial Pressure (MAP) or the use of vasopressors is measured.
Q7: What objective measurement evaluates the central nervous system in the SOFA score?
A7: The Glasgow Coma Scale Score is utilized.
Q8: What objective measurement evaluates renal function in the SOFA score?
A8: The creatinine level in mg/dL or urine output is measured.
Q9: What SOFA point value is given for a platelet count of < 100,000?
A9: A point value of 2 is assigned.
Q10: What SOFA point value is given for a Glasgow Coma Scale score of 13-14?
A10: A point value of 1 is assigned.
21. SEVERE SEPSIS AND SEPTIC SHOCK
Q1: What is the definition of Severe Sepsis?
A1: Severe sepsis is defined as sepsis accompanied by acute organ dysfunction.
Q2: What specific link must a provider document to assign a severe sepsis code?
A2: Provider documentation must explicitly link an acute organ dysfunction with sepsis to assign the severe sepsis code.
Q3: Should severe sepsis be coded if the link to acute organ dysfunction is unclear?
A3: Do not assign a severe sepsis code if the acute organ dysfunction is not clearly associated with the sepsis; if unclear, query the provider.
Q4: How is septic shock defined?
A4: Septic shock is defined as persisting hypotension requiring vasopressors to maintain MAP greater than 65 mmHg and having a serum lactate level greater than 2 mmol/L despite adequate volume resuscitation.
Q5: Name two organ dysfunction variables used to identify severe sepsis.
A5: Variables include a P/F ratio less than 300 and a creatinine increase greater than 0.5.
Q6: What finding regarding bowel sounds indicates organ dysfunction in severe sepsis?
A6: An ileus with absent bowel sounds indicates organ dysfunction.
Q7: What coagulation values indicate organ dysfunction in severe sepsis?
A7: An INR greater than 1.5, a PTT greater than 60 seconds, or thrombocytopenia less than 100K indicate organ dysfunction.
Q8: What lactate level indicates septic shock when combined with refractory hypotension?
A8: A lactate level greater than 4.0 indicates septic shock.
Q9: Is septic shock considered an MCC or CC?
A9: Septic shock is classified as an MCC.
Q10: Is severe sepsis alone considered an MCC or CC?
A10: Severe sepsis alone is classified as neither a CC nor an MCC.
22. SHOCK
Q1: What is the definition of shock?
A1: Shock is a pathophysiologic state of generalized inadequate tissue perfusion causing cellular hypoxia, typically associated with profound, refractory hypotension.
Q2: What are the vascular resistance components that can lead to shock?
A2: Components include peripheral vasoconstriction causing tissue hypoxia, or peripheral vasodilation exceeding cardiac capacity to maintain blood pressure and tissue perfusion.
Q3: What systolic blood pressure (SBP) indicates hypotension refractory to fluid resuscitation?
A3: An SBP of less than 90 mmHg indicates it.
Q4: What Mean Arterial Pressure (MAP) defines shock?
A4: A MAP of less than 70 mmHg defines it.
Q5: What drop in baseline SBP serves as a diagnostic criterion for shock?
A5: A decrease in baseline SBP of 40 mmHg or more serves as a criterion.
Q6: What lab value is equivalent to shock without blood pressure parameters?
A6: A lactate level greater than 4 mmol/L is equivalent to shock.
Q7: How is MAP alternatively measured in many modern settings?
A7: Many current external blood pressure monitors now incorporate MAP calculating technology, offering an alternative to traditional intra-arterial monitoring.
Q8: How is unspecified shock coded?
A8: Unspecified shock is coded as a CC.
Q9: How is post-procedural cardiogenic shock coded?
A9: It is coded as an MCC.
Q10: What are some specified types of shock listed that are coded as MCCs?
A10: Types include cardiogenic, hypovolemic, hemorrhagic, post-traumatic, and septic shock.
23. SIRS NON-INFECTIOUS
Q1: What condition is defined as SIRS due to causes other than infection?
A1: It is defined as non-infectious SIRS.
Q2: How many criteria must be met to diagnose SIRS?
A2: Fulfilling at least two of the four criteria is required.
Q3: What temperature values fulfill the SIRS criteria?
A3: A temperature greater than 38C (>100.4 F) or less than 36 C (96.8 F) fulfills it.
Q4: What heart rate fulfills the SIRS criteria?
A4: A heart rate greater than 90/min fulfills it.
Q5: What respiratory rate fulfills the SIRS criteria?
A5: Tachypnea with a respiratory rate greater than 20/min fulfills it.
Q6: What WBC counts fulfill the SIRS criteria?
A6: Leukocytosis with a WBC greater than 12K, less than 4K, or bands greater than 10% fulfills it.
Q7: How is SIRS with acute organ dysfunction classified for coding?
A7: It is classified as an MCC.
Q8: How is SIRS without acute organ dysfunction classified for coding?
A8: It is classified as a CC.
Q9: What should be done if it is unclear whether acute organ dysfunction is associated with SIRS or another condition?
A9: The provider should be queried.
Q10: What are some causes of non-infectious SIRS?
A10: Causes may include pancreatitis, trauma, malignancies, bowel infarction, extensive burns, major surgical procedures, and tumor lysis syndrome.
24. SKIN/PRESSURE ULCERS
Q1: How are non-pressure chronic ulcers defined?
A1: They are defined as an erosion of the epidermis or dermis that may extend to subcutaneous fat, fascia, muscle, ligaments, tendons, and bone, persisting for three months or more.
Q2: How are pressure ulcers defined?
A2: Pressure ulcers are defined as localized damage to the skin and/or underlying soft tissue due to intense or prolonged pressure, often associated with immobility and/or absent sensation.
Q3: What other factors contribute to pressure ulcers?
A3: Moisture and nutritional deficiency, or obesity, also contribute.
Q4: What is a Stage 1 pressure ulcer?
A4: It is characterized by non-blanching erythema of intact skin, which may appear differently in darkly pigmented skin.
Q5: What does "blanching" mean in normal skin?
A5: Normal skin turns pale when pressed with a finger, then promptly returns to its normal color because blood is squeezed out of capillaries and quickly refills when released.
Q6: What is exposed in a Stage 2 pressure ulcer?
A6: It involves partial thickness skin loss exposing the vascular dermis, but subcutaneous adipose tissue and deeper tissues are not exposed.
Q7: What does the wound bed look like in a Stage 2 pressure ulcer?
A7: The wound bed is viable, pink, or red, and moist; it may also present as an intact or ruptured serum-filled blister.
Q8: What is exposed in a Stage 3 pressure ulcer?
A8: It involves full thickness skin loss in which subcutaneous adipose tissue is exposed and visible, but fascia, muscle, tendon, ligament, cartilage, and bone are not exposed.
Q9: What is exposed in a Stage 4 pressure ulcer?
A9: It involves full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone.
Q10: What is a Deep Tissue Pressure Injury (DTPI)?
A10: It is intact or non-intact skin with a localized area of persistent non-blanchable deep red, maroon, purple discoloration, or epidermal separation revealing a dark wound bed or blood-filled blister.