Arterial blood gas can be obtained from a needle puncture from the radial, brachial, femoral, axillary, dorsalis pedis artery; or from an indwelling arterial catheter. It can measure the partial pressure of carbon dioxide (PaCO2), partial pressure of O2 (PaO2), and acidity. Then from those values we can calculate: bicarbonate and Arterial oxygen saturation (SaO2).Contraindications for obtaining ABG include: a failed Allen’s test, and infection/scarring/AV fistulas at the sample location. Its collection can be very painful, and risk scarring/ clotting/ aneurysms at the collection site. Also, it may be difficult to collect when patients have low pulses.

Some error may be a falsely lowered partial pressure of O2 (PaO2) when the sample is in room temperature. One reason for this is that O2 in the sample can be used up by the leukocytes or platelets, especially if the patients have an abnormally excessive level of them. Placing the sample on ice and having it analyzed within 15min helps avoid this error. Also, gas may diffuse out and give erroneous readings if a plastic syringe, and not a glass syringe is used.
Heparin can be added to the sample syringe to avoid coagulation, however, it can also cause issues. Its acidity may contribute to further reducing the sample’s pH. To avoid this, minimal heparin should be used, and at least 2mL of arterial blood should be collected.
Also, we must try to remove air bubbles after collecting the sample, since their presence can falsely elevate the partial pressure of O2 (PaO2), and falsely decrease the partial pressure of carbon dioxide (PaCO2).

Venous blood gas can be obtained from different sites: via venipuncture, central venous catheter, or from a pulmonary artery catheter. The correlation with ABG versus VBG is best studied with central venous blood gases, but venipuncture is typically used for those critically ill patients with no central access.
VBG can measure venous carbon dioxide tension (PvCO2), acidity (pH), oxyhemoglobin saturation (SvO2), and serum bicarbonate (HCO3) concentration.
Checking for the venous CO2, bicarbonate, and pH helps with checking acid-base status and ventilation. Oxyhemoglobin saturation (SvO2) is used to check the effectiveness of resuscitation in patients with sepsis or shock.

The values between ABG and VBG correlate well, and are helpful in determining acid base imbalances. Only exception is that VBG cannot measure one’s oxygenation like an ABG can, so its use is usually combined with pulse oximetry. With that said, ABG is especially preferred in patients who are hypoxemic, in shock, has ARDs, or has poor circulation that result in inaccurate pulse ox readings.

• https://www.uptodate.com/contents/venous-blood-gases-and-other-alternatives-to-arterial-blood-gases?search=blood%20gas%20interpretation&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2
• https://www.uptodate.com/contents/arterial-blood-gases?search=blood%20gas%20interpretation&topicRef=16991&source=see_link#H10
• https://www.youtube.com/watch?v=oVoJgd3DR5U
• https://epmonthly.com/article/blood-gases-abg-vs-vbg/

Alanine aminotransferase (ALT)(normal Male: 29 to 33 units/L, Female: 19 to 25 units/L), Aspartate aminotransferase (AST)(normal Male: 10 to 40 units/L, Female: 9 to 32 units/L), and Alkaline phosphatase (ALP)(normal Male: 45 to 115 units/L, Female: 30 to 100 units/L) are used as biomarkers of liver injury. AST is present in the liver, heart, skeletal muscle, kidney, and brain; while ALT is primarily found in the liver, making it a more specific marker for injury to the liver. ALP is found in the liver and bones. Elevations of AST and ALT are more associated with hepatocellular issues, while elevations of ALP is more associated with cholestasis. If all these biomarkers are elevated, the larger abnormality will indicate where the issue is caused by.When the liver is damaged, AST and ALT are released from the hepatocytes. The amount of elevation of their values in the serum may indicate what is causing the liver injury. For example, <4x normal value tends to be from nonalcoholic fatty liver disease; while ALT <5x and AST <8x normal values indicates alcoholic fatty liver disease (AST 2: ALT 1 ratio, liver impairing B6 which is necessary to sysntesisze these, extreme elevations points away from alcoholic issue). Over 15x normal may show acute liver failure. Elevations of both aminotransferase values above 25x normal value can show viral hepatitis or toxin-caused hepatitis. And elevations above 50x normal value can show some kind of ischemia, (HF from hypoperfusion of liver), or shock in the liver.

The degree of aminotransferase elevation may point to different differentials, as well as course of management. With elevations less than 15x normal values, differentials that can be considered are chronic viral hepatitis, medications, hemochromatosis, alcoholic liver disease, thyroid disorders, adrenal insufficiency, anorexia nervosa, and more. Part of evaluating these patients would be to review medications and other possible drugs, check for alcohol abuse, draw hepatitis panels, draw serum iron and TIBC to evaluate for hemochromatosis, and potential liver U/S or CT to check for fatty liver. In well-appearing patients with elevations less than 5x normal limit, they can be monitored over 3-6 months.

With severely elevated levels, differentials can include acetaminophen toxicity, other toxin exposure, acute viral hepatitis, alcoholic/autoimmune/ischemic hepatitis, Budd Chiari syndrome, sepsis, and more. Evaluation may include getting acetaminophen levels, toxicology screening, hepatitis panel, and autoimmune markers, with possible further investigation with U/S to look for evidence of no perfusion to the liver, and liver biopsy.

Elevations 4x above normal value of ALP are typically are seen in cholestasis. Elevation due to hepatic issues can be confirmed with gamma-glutamyl transpeptidase (GGT) and serum 5′-nucleotidase levels; since their values are also elevated when there’s a liver issue and not a bone issue. As mentioned before, ALP is more associated with cholestasis, which involves the impaired formation and secretion of bile. Common causes include intra or extrahepatic occlusion of bile ducts, biliary cholangitis, sclerosing cholangitis, sarcoidosis, and certain drugs (ie: phenytoin). Initial evaluation will include RUQ U/S. From visualizing biliary dilation, it would indicate extrahepatic cholestasis. To confirm, ERCP, MRCP or CT can be done to search for what is causing the obstruction. The lack of biliary dilation on U/S would require further evaluation (antimitochondrial Ab (AMA), antinuclear Ab, antismooth muscle Ab, liver biopsy) to confirm possible causes of intrahepatic cholestasis (ie: drug toxicity, biliary cholangitis, viral hepatitis).

https://www.uptodate.com/contents/approach-to-the-patient-with-abnormal-liver-biochemical-and-function-tests?search=ast&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Chorioamnionitis

The placenta is made of multiple layers, the outermost is referred to the “chorion”, and the innermost is referred to as the “amnion”. Within the amnion contain the fetus and amniotic fluid. Chorioamnionitis refers to inflammation that is present either at the chorion, amnion, or both. However since infection can also involve the fetus, amniotic fluid, or umbilical cord, with medical complication can be referred to as IAI, intra-amniotic infection.

It is mainly caused by the rupture of the amniotic sac, where polymicrobial flora from the vagina or cervix ascending through the cervical canal to cause infection. However it can also occur if the mother has bacteremia, or if the mother had an invasive procedure that might expose the amniotic cavity to pathogens. Normally, the cervical mucous plug and placenta, mother’s vaginal flora, and immune responses from the fetal membrane, can prevent this infection.

In chorioamnionitis, labor should be induced to deliver the baby and other products of conception. If C-section is considered, be aware that it may cause increased risk of infection at the wound, venous thrombosis, and endomyometritis. In conjunction with delivery, broad spectrum antibiotics should be given. UpToDate suggests the combination of IV Ampicillin 2g Q6hr and IV Gentamycin 5mg/kg QD. Other alternative antibiotics include Unasyn (Ampicillin/Sulbactam), Timentin (Ticarcillin/Clavulanic potassium), Zosyn (Piperacillin/Tazobactam), Cefoxitin, Cefotetan, and Ertapenem. Additional anaerobic coverage, such as Metronidazole or Clindamycin, should be added to the patients regimen when C-section is performed to reduce infectious complications. In fever, the mothers can be given acetaminophen.

Source:
https://www.uptodate.com/contents/intra-amniotic-infection-clinical-chorioamnionitis-or-triple-i?search=chorioamnionitis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Cystic teratoma / Dermoid cyst

Teratomas fall under the category of “ovarian germ cell tumors”, or tumors that arise from the reproductive cells. Teratomas are the MC type of germ cell tumor. Mature teratomas aka Mature cystic teratoma aka Dermoid cysts are the most common ovarian tumor in women in their 20-30s. They are benign, and made from mature/differentiated tissues that are derived from the 3 cell layers: ectoderm, mesoderm, and endoderm. The types of tissues may be found in the dermoid cyst include: skin, sebaceous glands, fluid, hair, teeth, bone, thyroid tissue, and muscle. Its formation is theorized to be because of abnormal differentiation of germ cells, or some failure in meiosis I or II.

Patients with dermoid cysts are typically asymptomatic. Symptoms may occur when the mass exceeds a certain size. Complications include torsion and rupture of the cyst, where the latter scenario may risk hemorrhage and shock.

The diagnosis of teratomas may be made initially with U/S. Some signs that may point to this diagnosis include: the visualization of a hyperechoic structure present within the mass, there being a fluid-fluid level, or there being some kind of calcification. Additional Doppler imaging should be done to help rule out other possibilities. If there is blood flow, other tumors, including malignant “immature” teratomas may be the issue. A definitive diagnosis can be made once the mass gets excised and histology studies are done.

The treatment of mature teratomas is to conduct ovarian cystectomy. The removal of the cyst itself would help to prevent torsion, rupture, and the potential of the tumor growing malignant parts. Those who do not plan to conceive anymore may consider salpingo-oophorectomy.

Source:
https://www.uptodate.com/contents/ovarian-germ-cell-tumors-pathology-epidemiology-clinical-manifestations-and-diagnosis?search=cystic%20teratoma&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H9
https://www.uptodate.com/contents/ultrasound-differentiation-of-benign-versus-malignant-adnexal-masses?search=cystic%20teratoma&topicRef=3236&source=see_link#H23239137

“Physical frailty” includes the signs and symptoms in the likes of fatigue, weakness, weight loss, and slow gait. “Deficit accumulation frailty” describes the complications of patients who have comorbid diseases/illnesses. With more physical and deficit accumulation frailties, these patients are considered more vulnerable and closer to having failure to thrive. It should be noted, however, that age is not used in frailty measurement since there are those older patients who are declining in function, while there are others who maintain their level of function.

It is important to assess for frailty in order to find out which patients are more at risk of adverse health outcomes and failure to thrive. This would create the opportunity for providers to work with the patient and their family in order to discuss treatment plans and the goals of caring for the patient. It is recommended for frailty to be screened in those patients who are over 70 years old, living with chronic diseases, or had had weight loss >5% in the past year.

Multiple screening tools exist to measure frailty. The Fried Frailty Tool is commonly used to measure physical frailty, which involves measuring the patient’s grip strength and walking speed, and taking into account weight loss, fatigue, weakness, and decreased physical activity. Deficit accumulation frailty can be measured with a questionnaire-like tool, which asks 20+ questions regarding the patient’s diseases, illnesses, decrease in cognition, and function. There is also the FRAIL mnemonic that allows for rapid assessment.

Score of 3-5 is frail, 1-2 is pre-fail.
Part of the frailty screening can also include checking if patients can rise from a chair 5x without the use of their arms, as well as walk across a room.

Sarcopenia, is defined as a “loss of skeletal muscle and muscle strength”. It can be the result of hormonal changes that occur with age. Sarcopenia can lead to decreases function, including slower walking speed, decreases aerobic endurance, loss of strength, and disability. It is associated with increased morbidity, mortality, and health care costs. To test for sarcopenia, this includes tests such as the grip strength, and walking speed as mentioned previously; and measurement of muscle mass.

• https://www.uptodate.com/contents/frailty?search=frailty&source=search_result&selectedTitle=1~147&usage_type=default&display_rank=1#H2
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297299/

Longterm concerns and preventive care for DKA

For preventive care in these patients, education is extremely important. These patients should be informed of proper dieting, exercising, and psychosocial maintenance. Greater parental involvement in the child’s diabetes care, check-ups, and treatments may also be needed.

When dealing with the patients’ nutrition, it may depend on whether or not they are on insulin. It is suggested that there should be controlled carbohydrate intake to lower the amount of sugars taken in; as well as education on proper foods/drinks.

The patient’s growth and development should be noted when starting insulin. Initially, the patients likely had weight loss from the uncontrolled diabetes. When insulin is started, the weight may be regained. If excessive insulin is given, the dose is not reduced after puberty, or the dose is not reduced after patient gains back the initial lost weight, the patient may become hypoglycemic. Therefore, it is important to keep monitoring the patient, and adjust the insulin dose if necessary. 

Exercise is encouraged in these patients, however, they need to be educated that the amount and intensity of exercise can lead to the body responding, and causing hypoglycemia within the following hours. It is suggested to have additional blood glucose monitoring around the time of exercise, as well as insulin dose adjustment.

Psychological issues should also be monitored. Children may run into issues from living with their chronic condition, and they may have stresses in school and their family. This can risk poor self-care, diet, and treatment adherence. It is important to address these sources of conflict in order to decrease the risk of hospitalizations and DKA.

Patients and their family should also be informed of the risk of untreated diabetes, or noncompliance with treatment. They should be educated that it can lead to the buildup of ketones and acids in the body, which can lead to DKA, and serious complications, like cerebral edema, cognitive impairment, pulmonary edema, DVT risk, organ damage, arrhythmias, or even death.

• https://www.uptodate.com/contents/management-of-type-1-diabetes-mellitus-in-children-and-adolescents?sectionName=OTHER%20MANAGEMENT%20ISSUES&search=dka%20management&topicRef=5808&anchor=H25&source=see_link#H25
• https://www.uptodate.com/contents/treatment-and-complications-of-diabetic-ketoacidosis-in-children-and-adolescents#H16

 

Reflection on the case presentations

DKA is a life-threatening complication seen in diabetics. I found it helpful when we reviewed its pathophysiology so that we could thoroughly understand how this problem occurs within the body. It mostly occurs in DM1 patients, whose bodies are unable to produce insulin. Insulin is important to allow glucose to enter cells for its usage. When the body lacks insulin, it will produce counterregulatory hormones (ie: glucagon, cortisol, GH) in order to produce alternative forms of energy. The liver will undergo gluconeogenesis, further increasing the glucose circulating in the blood. Triglycerides will get broken down into free fatty acids, which then will break down into ketones. The buildup of ketones can be seen in blood and urine, making the blood acidic. The complications of DKA were also covered: cerebral edema, cognitive deficits, DVT risk, and increased pancreatic enzymes.

We reviewed the treatment goals of DKA, which included: correcting dehydration with IV fluids, giving insulin to reduce ketosis and hyperglycemia, and correcting electrolyte imbalances. Learning how to calculate the amount of NS or LR to give when treating dehydration and fluid maintenance was challenging, but useful as an introduction of how to do it. Some takeaways were: 1kg of weight loss = 1L of fluid depleted; 10-20mL/kg via IV bolus is given initially in pediatric DKA, while 15-20mL/kg can be given in adults; 0.1unit/kg/hr IV insulin infusion should be given in peds, while 0.1 units/kg IV bolus of regular insulin, followed by 0.1 units/kg/hour continuous infusion should be given in adults; electrolyte imbalances (ie: Na, K, phosphate, Ca, Mg) need to be monitored for and corrected; and that bicarbonate can be given in adults with DKA, but not in pediatric DKA patients.

Last but not least, we covered the concept of anion gap. In our plasma, we need the charges to add up to be electrically neutral. The measurement of anions and cations concentrations in the plasma is difficult, so the equation of anion gap is used. Na – (HCO3- + Cl-). It describes how much more positive cations there are from negative anions, which is usually 8-12mEq/L. The gap is present since Na+ accounts for the majority of positive charges, while the equation does not account for some of the negative charges that exist beyond Cl- and HCO3- concentrations, such as organic acids and negatively charged proteins.

History:
81 year old female with PMHx Hypothyroidism, HDL, dementia, and PE on Xarelto, presents to the ED today sent in from NH s/p fall. Patient is A&O x 2 and is unable to give full history or ROS. Denies falling, fever, or difficulty breathing; however, as per triage note, patient was sent in s/p fall with noted to have temp 39.2 of Patient was noted to be hypoxic on RA, then placed on 4L of O2 via NC. 

Physical:
SKIN: Warm, dry; (-) cyanosis; (-) rash.
HEAD: (-) scalp swelling, (-) tenderness.
EYES: (-) conjunctival pallor, (-) scleral icterus, (+) EOMI
ENMT: Pharynx: (-) erythema; airway patent: (-) stridor; mucous membranes moist.
NECK: (-) tenderness, (-) stiffness
CHEST AND RESPIRATORY: (-) rales, (-) rhonchi, (-) wheezes; breath sounds equal bilaterally.
HEART AND CARDIOVASCULAR: (-) irregularity; (-) murmur, (-) gallop.
ABDOMEN AND GI: Soft; (-) tenderness, (-) guarding, (-) rebound (+) slightly distended
EXTREMITIES: (-) deformity, (-) edema, (-) tenderness, (+) full range of motion, (+) equal pulses in upper and lower extremities
NEURO AND PSYCH: Mental status as above.

Steps to rule out cardiac differential diagnoses:
Labs: CBC, CMP, Lipid panel, Troponin, CK-MB, BNP, NT-proBNP, blood culture (possible endocarditis)
Imaging: ECHO (look at ejection fraction, abnormal blood flow), CXR (possible CHF, PE, Pneumonia)

Pertinent Findings:
Xray: Patchy ground glass opacities along the periphery with the largest in the right upper lobe. Although nonspecific this is suggestive of atypical pneumonia.

Treatment Plan:
Maintain 4L of O2 via NC
Administer 0.9% sodium chloride via IV over 2 hours
Treatment of atypical pneumonia: Azithromycin x 7 days (500mg on first day, 250mg from days 2-5)
Monitor for target urine output of 0.5-1ml/kg/hr
Check vitals and obtain serial labs Q 8 hours

 

Significance of troponins and proBNP, what is EF, HFrEF vs HFpEF
Troponin I
Significance: released when there is damage to heart muscle, cardiac specific, rises 3-12 hour after MI, peaks at 24 hours and can stay elevated for days
Normal range: 0.00 – 0.045ng/mL
Lab results: 0.045 > 0.031 >0.010ng/mL
Shows improvement over time, falling into normal range, suggesting less risk/chance of cardiac ddx
Also note: troponin can be falsely positive in renal failure

NT-proBNP (N-terminal-prohormone BNP)(non-active prohormone that is released from the same molecule that produces BNP)
Significance: BNP and this prohormone are produced when the heart is undergoing stress or stretch, they are released from ventricles, elevated in CHF, can help diagnose HF; helps in determining prognosis of patients with heart failure, coronary artery disease, and valvular heart disease
Normal range: <125pg/mL normal, >500 HF?
Lab results: 231
Note: other conditions that proBNP can be elevated are obesity, constrictive pericarditis, pericardial effusion, and flash pulmonary edema
Possible that theres elevated proBNP from pulmonary edema secondary to pneumonia

Ejection fraction: measures the amount of blood that is pumped out of the LV during each contraction, normal range is 55-75%, During HF, EF can either be reduced (HFrEF) or preserved (HFpEF)
In reduced (MC), <55% of blood is being pumped with each contraction, systolic dysfunction
Can be caused by enlarged LV (so big, heart cant pump normally), CAD or MI (limited blood flow to heart can damage/weaken it), HTN or Aortic stenosis (heart puts in more work to pump against pressure/valve, which weakens it), Mitral regurgitation (leakage of blood from LV to LA will stretch/weaken heart), arrhythmias (can affect amount of blood being pumped out)
In preserved, EF remains in normal range, diastolic dysfunction
Can be caused by enlarged LV (so big, heart fill normally), CAD or MI (limited blood flow to heart can damage walls and prevent relaxation for filling to occur), chronic HTN or Aortic stenosis (heart muscle thickened from working too much, now it cant fill); pericardial tamponade, or pericardial scarring can limit filling

Sources:
Diagnostic Studies (Laboratory Medicine) slides – Summer 2019 https://www.uwhealth.org/health/topic/special/heart-failure-with-reduced-ejection-fraction-systolic-heart-failure/tx4090abc.html
https://www.uofmhealth.org/health-library/tx4091abc
http://atm.amegroups.com/article/view/28884/html