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Postpartum Hemorrhage (PPH)

1/30/2024

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Postpartum hemorrhage (PPH)

Postpartum hemorrhage (PPH) is defined as severe vaginal bleeding after childbirth.
It is a serious condition that can lead to death.

Primary PPH occurs within the first 24 hours after delivery, while secondary or late PPH occurs 24 hours to 12 weeks postpartum.

Background

Traditionally, PPH has been defined as greater than 500 mL estimated blood loss associated with vaginal delivery or greater than 1000 mL associated with cesarean delivery.
PPH is considered an obstetric emergency and is one of the top five causes of maternal mortality in both resource-abundant and resource-limited settings.

Etiology

The most common causes of PPH are related to the 4T:
Tone: Uterine atony is the most common cause of PPH. This occurs when the uterus fails to contract firmly after childbirth, which can lead to excessive bleeding.
Trauma: Vaginal or cervical tears, or uterine rupture can also cause PPH. These injuries can occur during labor and delivery, especially if the birth is prolonged or difficult.
Tissue: Retained placenta or clots can also lead to PPH. If the placenta is not completely expelled after childbirth, or if there are large blood clots in the uterus, this can cause continued bleeding.
Thrombin: Pre-existing or acquired coagulopathy can also contribute to PPH. This occurs when there is a problem with the blood's ability to clot, which can lead to excessive bleeding.

Clinical presentation

The clinical presentation of PPH can vary based on the severity of bleeding. Common signs and symptoms include:
Excessive or persistent vaginal bleeding, hypotension, tachycardia, tachypnea, pallor, diaphoresis, altered mental status, and uterine atony, that is, failure of the uterus to contract effectively.

Management of Postpartum Hemorrhage:

Initial Resuscitation:

Activate the OB-GYN team immediately.
Establish two large-bore intravenous lines to ensure adequate fluid resuscitation.
Activate the massive transfusion protocol as needed to ensure that blood products are readily available.
Administer uterotonics to stimulate uterine contractions and help control bleeding.
Administer tranexamic acid 1 gram intravenously every 8 hours for 24 hours to reduce blood loss.
Administer fibrinogen to correct any clotting abnormalities.

Compression:

Perform bimanual uterine massage to stimulate uterine contractions and help control bleeding.
Insert a uterine balloon tamponade to tamponade the bleeding.
Manually reduce uterine inversion if it has occurred.

Surgery and Intervention:

If conservative measures fail to control bleeding, surgery may be necessary.
Hysterectomy may be necessary in severe cases.
Uterine artery ligation may be performed to control bleeding.
B-Lynch suture may be used to compress the bleeding site.
Transarterial embolization (TAE) is a minimally invasive procedure that involves injecting embolic material into the uterine arteries to block blood flow and control bleeding.

Uterotonics for PPH:

Oxytocin:
Initially 10 units intravenously, then 10 to 40 units per minute as needed.

Misoprostol:

800 to 1000 micrograms orally, sublingually, or rectally, every 4 to 6 hours as needed.

Methylergonovine:

0.2 milligrams intramuscularly or intravenously, every 2 to 4 hours as needed.

Carboprost:

250 micrograms intramuscularly every 15 min to a maximum of 8 doses as needed.

Active Management of 3rd Stage Labor:

Identify risk factors such as PPH history, grand multiparity, primigravida, macrosomia, polyhydramnios, multiple gestations, prolonged or augmented labor, and chorioamnionitis.
Establish 2 intravenous accesses.
Have blood available for transfusion.
Have uterotonic and intravenous fluid by the bedside.
Develop a Mother-Child Care Set. Include essential supplies and medications for both the mother and the newborn, facilitating prompt and organized intervention.
Administer oxytocin immediately after delivery and provide uterine massage.
Allow spontaneous delivery of the placenta or perform controlled cord traction.
Strict follow up in the first 2 hours postpartum.

Take Home Message:

Consider to transfer PPH patients for definitive management.
Transfer patient to operating room for hysterectomy or uterine artery ligation.
This is probably the most readily available option.

Transfer patient to interventional radiology for uterine artery embolization, for stable patients, as an attempt to maintain fertility.

Monteggia and Galeazzi Fractures

1/28/2024

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Monteggia and Galeazzi Fractures

The Monteggia fracture is a fracture of the proximal ulna associated with dislocation of the radial head.
The Galeazzi fracture is a fracture of the middle to distal third of the radius associated with dislocation or subluxation of the distal radioulnar joint (DRUJ).
The M-U-G-R mnemonic is a helpful way to remember the difference between Monteggia and Galeazzi fractures, both of which involve forearm bone fractures and dislocations.
M-U reminds that Monteggia fracture involves the ulna bone.

G-R reminds that Galeazzi fracture involves the radius bone.

Sgarbossa criteria

1/27/2024

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Sgarbossa criteria

Sgarbossa criteria is vital for the early detection of “STEMI” in patients with left bundle branch block or paced ECG rhythms. Sgarbossa criteria consist of three key indicators.
First, concordant ST segment elevation of 1mm or more in any lead, which scores 5.
Second, ST segment depression of 1mm or more in any lead from V1 to V3, scoring 3.
Third, discordant ST segment elevation of 5mm or more in any lead, scoring 2 if present. A score of 3 or more is highly specific, although it may be less sensitive.
The modified Sgarbossa criteria is positive for “STEMI” if there is discordant ST elevation with amplitude > 25% of the depth of the preceding S-wave.

Fournier's gangrene

1/21/2024

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Fournier's gangrene:

Rapidly progressive necrotizing fasciitis involving the perineum, genitalia, and perianal areas.
Polymicrobial: group A Streptococcus, Staphylococcus aureus, and anaerobic bacteria.
Pain, erythema, and swelling of the perineum, genitalia, and perianal areas, fever, bullae, crepitus.
Broad-spectrum antibiotics, surgical debridement of necrotic tissue, and supportive care.

Tumor Lysis Syndrome

1/19/2024

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Tumor Lysis Syndrome

Introduction

Tumor lysis syndrome is a life-threatening metabolic emergency that occurs when cancer cells are rapidly destroyed, releasing their contents into the bloodstream. This can happen spontaneously or as a result of chemotherapy, radiation therapy, or surgery.
Tumor lysis syndrome is characterized by a constellation of metabolic abnormalities, including hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, azotemia, and oliguria.
If left untreated, Tumor lysis syndrome can lead to cardiac arrhythmias, seizures, renal failure, and death. The Table on the left shows laboratory findings that are commonly used to diagnose tumor lysis syndrome.

Causes of Tumor Lysis Syndrome

The most common types of cancer that can cause Tumor lysis syndrome are: Leukemia, Lymphoma, Burkitt's lymphoma, Acute myeloid leukemia, Small cell lung cancer, Breast cancer, Ovarian cancer, and Testicular cancer.
Tumor lysis syndrome is more likely to occur in patients with: High tumor burden, Rapidly growing tumors, Tumors that are sensitive to chemotherapy or radiation therapy, and Pre-existing renal dysfunction. The Table on the left is a list of risk factors associated with Tumor lysis syndrome.

Pathophysiology

The pathophysiology of Tumor lysis syndrome is complex and involves a cascade of events that are triggered by the release of cellular contents from rapidly lysed cancer cells.
These cellular contents include potassium, phosphate, uric acid, and other metabolites. The accumulation of these metabolites, if left untreated, can lead to cardiac arrhythmias, seizures, renal failure, and death.

Hyperkalemia.

The release of potassium from lysed cancer cells can lead to hyperkalemia, which can cause cardiac arrhythmias and sudden death.

Hyperphosphatemia.

The release of phosphate from lysed cancer cells can lead to hyperphosphatemia, which can precipitate as calcium phosphate crystals in the kidneys, causing acute kidney injury, renal failure, and hypocalcemia.

Hypocalcemia.

Hypocalcemia can occur as a result of hyperphosphatemia, which binds to calcium and forms insoluble calcium phosphate complexes. Hypocalcemia can cause neuromuscular irritability and seizures.

Hyperuricemia.

The release of uric acid from lysed cancer cells can lead to hyperuricemia, which can cause uric acid crystallization in the kidneys and renal failure.

Azotemia.

Azotemia is the accumulation of nitrogenous waste products in the blood, such as urea and creatinine. Azotemia and oliguria can occur as a result of renal failure.

Clinical Manifestations

The clinical manifestations of Tumor lysis syndrome can vary depending on the severity of the condition. However, some of the most common symptoms include: Nausea, Vomiting, Diarrhea, Abdominal pain, Muscle weakness, Seizures, Coma, Cardiac arrhythmias, and Renal failure.

Diagnosis

Tumor lysis syndrome is diagnosed based on a combination of clinical symptoms and laboratory findings.
The following laboratory tests are typically used to diagnose Tumor lysis syndrome: Serum potassium, Serum phosphate, Serum calcium, Serum uric acid, Blood urea nitrogen, and serum Creatinine. The Cairo-Bishop criteria defines Tumor lysis syndrome as the presence of at least two metabolic disturbances within 3 days before or 7 days after initiation of therapy.

Treatment

The treatment of Tumor lysis syndrome is aimed at correcting the metabolic abnormalities and preventing complications. The following treatments are typically used:
Intravenous fluids to correct dehydration and electrolyte imbalances.
Allopurinol works by inhibiting xanthine oxidase, the enzyme responsible for converting hypoxanthine to uric acid.
Rasburicase is a recombinant version of the enzyme urate oxidase, which enhances the conversion of uric acid to a soluble metabolite, allantoin.
Both Allopurinol and Rasburicase are effective in lowering serum uric acid level.
Sodium bicarbonate to alkalinize the urine and prevent uric acid crystallization.
Dialysis to remove waste products from the blood.
It is generally not recommended to supply calcium to these patients, as this can increase the calcium phosphate product and lead to further renal deposition and damage.

Prevention

The best way to prevent Tumor lysis syndrome is to identify patients at risk and start treatment before the condition develops. Patients at risk for Tumor lysis syndrome should be given prophylactic treatment with allopurinol or rasburicase before starting chemotherapy or radiation therapy. It is also advisable to avoid substances that can potentially cause vasoconstriction of the renal vasculature, such as NSAIDs and iodinated contrast.

Conclusion

Tumor lysis syndrome is the most common oncologic emergency. This condition is prevalent in both adult and pediatric oncology patients undergoing chemotherapy, though it can also occur spontaneously.
Most of the symptoms seen in patients with tumor lysis syndrome are related to the release of intracellular chemical substances that cause impairment in the functions of target organs.

The accumulation of these metabolites, if left untreated, can lead to cardiac arrhythmias, seizures, renal failure, and death.

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