Hypertension In Pregnancy

Preeclampsia

It's critical to keep an eye out for organ failure and superadded preeclampsia in pregnant individuals with hypertension.

Risk Factors For Preeclampsia

Maternal Obstetric Risk Factors

• Nulliparity
• Multiple gestational pregnancies (twins, triplets)
• History of previous preeclampsia
• Prior intrauterine growth restriction in the previous child
• Prior placental abruption
• Any artificial reproductive technology used
• Molar pregnancy
• Trisomy 13
• Foetal hydrops
• Gestational diabetes

Paternal Obstetric Risk Factors

The father was born into a preeclamptic pregnancy; preeclampsia runs in the family.

Maternal Comorbid Conditions

• Hypertension
• CKD
• Diabetes
• Obesity
• APLA syndrome
• SLE
• PCOD

Maternal Genetic Risk Factors

• Thrombophilia
• Preeclampsia in a first-degree relative

Other Maternal Risk Factors

• Age older than 40 years
• born small for gestational age
• Mother is small for gestational age
• Pregnancy interval greater than ten years

Reduced Risk Factor

Smoking. It is not recommended to smoke while treating preeclampsia since it can increase hypertension and result in prenatal abnormalities.

Pathogenesis Of Preeclampsia

Preeclampsia is a maternal endothelial condition that is brought on by the placenta, not the fetus.There are two phases to it:
1. Hypoxia or placenta ischemia.
2. Reproduction harm from ischemia that causes inflammation in the mother. Multiple organ involvement and dysfunction result from maternal inflammation.

Possible Pathogenetic Mechanisms of Preeclampsia

 In general, aberrant angiogenic factor levels and placental dysfunction are the immunological causes of preeclampsia.
  A key TGF beta receptor called soluble endoglin increases the release of PGF beta. Reactive oxygen species and hypertension may also result from the formation of an angiotensin one anti-receptor antibody.

Imbalance of Angiogenic and Antiangiogenic factors

• ↑ antiangiogenic factors
• sFlt – 1 binds to VEGF, PIGF
• sEng – coreceptor of TGF-β
• AT1AA – ROS, Hypertension

Preeclampsia is caused by a combination of immunological mechanisms, aberrant trophoblasts, genetic predisposition, and maternal risk factors.  These variables result in poor spiral artery remodeling, improper placental positioning, and mismatch in placental oxygen requirement.

This results in an imbalance of angiogenic factors, hypoxia, and oxidative stress.  In addition to other mediators like the sympathetic nervous system, uric acid, and vasopressin, inflammatory cytokines are released.  End-organ injury and maternal endothelial dysfunction result in vasoconstriction, activated leukocytes and endothelial cells, and reduced nitric oxide.

Hypertension, proteinuria, AKI, aberrant LFTs, liver rupture, seizures, strokes, visual abnormalities, pulmonary edema, IUGR, and fetal death are among the clinical characteristics of preeclampsia.

Renal Abnormalities in Preeclampsia

Pathology: Endothelial dysfunction; Glomerular endothelins: Swelling and vacuolization of endothelial cells due to damage; Glomerular capillary occlusion: Tuft ischemia and glomerular enlargement due to swollen endothelial cells; Immunofluorescence: Fibrin deposits are visible; Reduced renal blood flow:

Primary pathology leading to increased sodium and uric acid reabsorption; Decreased renin release and prostaglandin: Because of increased reabsorption; Reduced GFR: As a result of the primary pathology stimulating sodium reabsorption and suppressing Renin angiotensin; Pathological findings: Proteinuria and endothelins; Glomerular endotheliosis is the pathological finding of preeclampsia.

Other Renal Features Seen In Preeclampsia

Clinical Features Of Preeclampsia

Primary Manifestation

• Hypertension
• Hypertension starting after 20 weeks of pregnancy

Renal Involvement

Significant proteinuria: > 30 mg/mmol (about > 300 mg/g creatinine) spot ratio of urine protein to creatinine confirms a positive dipstick result.  Serum or plasma creatinine > 90 mmol/l indicates acute renal damage.  Liberia

Hematologic Involvement 

• Thrombocytopenia
• Hemolysis
• Disseminated intravascular coagulation

Liver Involvement

Raised serum transaminases Severe epigastric or right upper quadrant pain

Neurological Involvement

Hyperreflexia with prolonged clonus; seizures (eclampsia); severe headache accompanied by hyperreflexia; persistent visual disruption (photopsia, scotomata, cortical blindness, retinal vasospasm)  Stroke or cerebrovascular accident

Other Major Features

• Pulmonary edema
• Fetal growth restriction
• Placental abruption 

Evaluation

Maternal evaluation: take blood pressure, monitor for symptoms, and conduct any necessary tests on the blood and urine to identify end organ damage.  Fetal assessment: routine ultrasonography to determine the amount of amniotic fluid surrounding the fetus and its growth.

Eclampsia

Seizures that occur during or after pregnancy and have no other explanation are the hallmark of epilepsy. Within the first five days following delivery, half of the instances occur. There is no correlation between BP level and eclampsia risk.
Even in the absence of proteinuria, epilepsy can happen.
  Photopsia, vision abnormalities, and epigastric discomfort are possible symptoms; headaches are the most prevalent premonitory sign. This is an exclusion diagnosis.

HELLP Syndrome

Hemolysis, Elevated Liver Enzymes, and Low Platelet Count is referred to as HELLP.  It belongs to the same spectrum as TMA and is a severe form of preeclampsia.  Hemolysis, indicated by decreased haptoglobin, increased LDH, and cystocytes in the urine, is necessary for the diagnosis.
• Increased liver enzymes (AST > 70).
• Low platelet count, usually less than 100,000
• There is a 1% chance of maternal death.
• There is a 7% to 34% increased chance of fetal death.

Also Read: Renal Physiology In Pregnancy

Natural History of Preeclampsia and its Complications

Presumptive hypertension may develop from gestational hypertension.  If gestational hypertension begins before 32 weeks, the risk of having preeclampsia is 33%; if it occurs after 36 weeks, the risk is 10%.
•Problems for the developing fetus:
• 10–25% is the intrauterine growth restriction (IUGR).
• Complications related to mothers: • AKI: 1-5%
• Liver participation: 10%–20%
• Neurological anomaly: less than 1%
• Edema pulmonary: <0.5%
• Preterm and perinatal deaths are uncommon.
• When preeclampsia is present, there is an elevated risk of thrombocytopenia and impaired liver function.

Prediction tools

The Sflt1/PIGF ratio is one of the prediction techniques that have been created for preeclampsia.  PIGF is any androgenic factor, such as VEGFt or PIGF, and Sflt1 is an antiangiogenic factor that rises in preeclampsia.  The presence of preeclampsia is indicated if the Sflt1/PIGF ratio is greater than 38.

A larger ratio suggests that a delivery is necessary.  Preeclampsia can also be predicted by the existence of copeptin. It is possible to perform a Doppler ultrasound on moms who have risk factors, as this test can also detect preeclampsia.

Also Read: Tropical Acute Kidney Injury

Preventing And Managing Preeclampsia

Prevention

To lower the chance of developing preeclampsia, aspirin can be administered to high-risk patients (those with CKD, chronic hypertension, or SLE).  Aspirin should be taken until 37 weeks, starting as early as 12–14 weeks. It is also advised to take calcium supplements to lower the risk of preeclampsia.

Management

Monitoring fetal tomography, liver enzymes (AST), serum creatinine, and platelet count is part of general care.
Since proteinuria testing does not indicate the severity of preeclampsia, it is not necessary to repeat it once proteinuria has been diagnosed.

Every two to three weeks, an umbilical artery doppler and USG should be performed.  Aspirin administration does not stop preeclampsia from getting worse. Gynecologists are the experts in treating preeclampsia effectively.

Preeclampsia complications include pulmonary edema, liver involvement, neurological problems, fetal development restriction, and maternal AKL.

Blood Pressure Management in Preeclampsia    

It's critical to control blood pressure to avoid preeclampsia complications such as placental abruption and stroke.
  Only the symptoms of the underlying condition are treated with BP management.  The target blood pressure range is 80–85 diastolic and 110–140 systolic.

When blood pressure exceeds 160/100, treatment is recommended.  Patients with hyperreflexia with clonus, excruciating headaches, and visual scotoma are treated with magnesium prophylaxis for seizures when their blood pressure is elevated.  Controlling blood pressure is crucial for avoiding preeclampsia problems.

 While treating hypertension can avoid problems like stroke and placental abruption, it does not treat preeclampsia.
If the patient exhibits symptoms like severe headache, visual scotoma, or hyperreflexia with clonus, and their blood pressure is high, they should be treated with magnesium for seizure prevention.

Because of possible side effects such pulmonary edema, ACE inhibitors, diuretics, and volume expansion are not recommended.

Also Read: Tropical Acute Kidney Injury

Treatment Options for Preeclampsia

 Dextran apheresis was an older treatment strategy that involved eliminating Sflt one from blood, but it was not proven to be particularly helpful and is not recommended. • Delivery of the placenta is the only effective treatment option for preeclampsia.

When there is increasing evidence of maternal organ dysfunction, such as elevated creatinine, anemia, and thrombocytopenia, delivery is indicated.  The inability to regulate blood pressure is another sign that a baby should be delivered since it increases the risk of stroke, seizures, placental abruption, and maternal death.

Indications of foetal growth include gestational age more than 37 weeks or severe IUGR.  The fetus is deemed stable at 37 weeks, at which point the placenta can be delivered.

Also Read: Alport Syndrome and Familial Glomerular Disorders

Management Of Preeclampsia

Delivery

If organ failure is absent and blood pressure is less than 160/110: Deliver the baby immediately.  If the pregnancy is more than 37 weeks along, schedule a normal delivery.
If the pregnancy is less than 37 weeks, the patient should be admitted for either inpatient or outpatient care, monitored for a full day, and then followed up as an outpatient with weekly blood tests, fetal development checks every three weeks, and blood pressure control.

If during monitoring there is any indication of organ dysfunction, end the pregnancy.

Postpartum Management of Preeclampsia

 Blood pressure should return to normal in three months following placenta removal; abnormalities, such as proteinuria, may take up to twelve months to resolve; recovery period is five to seven days.

15% of recurrences in subsequent pregnancies  The recurrence rate for preeclampsia cases that occurred prior to 28 weeks is approximately 25%.

Long-term Consequences of Preeclampsia

• Fatal and non-fatal coronary heart disease
• Stroke
• Hypertension
• Thromboembolism
• Increased risk of end-stage renal disease (ESRD)
• Increased risk of developing diabetes
• Cognitive dysfunction
• White matter lesions on cerebral CT
• Death

Acute Fatty Liver Of Pregnancy

• Risk factors
  • Primigravida pregnancy
  • Multiple gestations
  • Male fetus
• Time of occurrence
  • Third trimester
• Importance of time of occurrence in diagnosis
• Clinically based question
• Symptoms and signs
  • Nausea
  • Vomiting
  • Abdominal pain
  • Jaundice
  • Encephalopathy
• Complications
  • Maternal mortality
  • Foetal distress
  • Preterm delivery

Pathogenesis Of Acute Fatty Liver Of Pregnancy (AFLP)

The autosomal recessive disorder AFLP is brought on by a functional deficit of the LCHAD enzyme in the developing infant.  The fetus's mitochondrial fatty acid oxidation process depends on the LCHAD enzyme.

The hallmark of AFLP is lipid microvesicle infiltration of hepatocytes;  Hemodynamic changes in HRS/TMA can cause renal involvement;  Fatty acids accumulate in the fetus and enter the maternal circulation, leading to hepatic dysfunction; •AFLP is primarily a deficiency in the fetus that affects the mother; it is not a primary maternal disorder.

Clinical Features Of Acute Fatty Liver Of Pregnancy(AFLP)

Fever, malaise, epigastric discomfort, nausea, vomiting, and jaundice resembling hepatitis are among the clinical characteristics of AFLP.  The degree of liver involvement might range from moderate to severe. Fifty percent of individuals with AFLP also have coexisting preeclampsia.  It's critical to distinguish AFLP from other illnesses because of the differences in treatment and the need for immediate attention.

Treatment And Mortality Rates Of Acute Fatty Liver Of Pregnancy

• Treatment: Supportive care, prompt delivery
• Complete renal and liver recovery occurs after delivery
• Maternal mortality rate: around 18%
• Perinatal mortality rate: around 55%
• Problem is primarily in the child, the mortality rate in children: is around 55%

TMA and Its Spectrum

 Thrombotic microangiopathy, or TMA, is typified by platelet and fibrin microformations in the microcirculation.  It is a spectrum condition that includes TTP, HUS, and HELLP syndrome.  HUS and TTP represent the worst end of the continuum, and HELLP syndrome represents the better end.

Hemolytic Uremic Syndrome is referred to as HUS.
Thrombotic Thrombocytopenic Purpura is referred to as TTP.
TTP occurs less than 28 weeks of pregnancy, whereas HUS occurs postpartum.  In TTP, coagulation tests and LFT are normal; in preeclampsia or HELLP syndrome, these parameters may be changed.  LDH: Because of hemolysis and a healthy liver, the AST ratio is typically more than 25:1 in TTP.

Clinical Features and Timing of Occurrence

Fibrin and platelet microthrombi in the microcirculation are the hallmark of TMA, which ranges from HELLP syndrome to HUS and TTP.  TTP is often observed in fewer than 28 weeks of pregnancy, whereas HUS typically occurs postpartum.
  Hemolysis causes the LDH to AST ratio to typically be greater than 25:1, and coagulation tests and LFT are normal in TTP.When diagnosing clinical-based concerns, it can be helpful to keep in mind the timing of the occurrence.

Natural History and Treatment

 TMA is a serious illness that has a 10- to 20% mother death rate and a 30- to 80% perinatal death rate. Treatment options include plasma infusion and plasmapheresis.

Acute Kidney Injury In Pregnancy

Since creatinine levels typically drop during pregnancy, any increase of more than one or 0.5 over baseline in the course of 48 hours should be treated as AKI.
There may be two AKI peaks: one in the first trimester and one in the third.

Treatment for AKI in pregnancy is based on its etiology and severity, and diagnosis of the condition should have a low threshold. AKI is categorized according to its site of occurrence: prerenal, renal, or postrenal.

Acute Cortical Necrosis In Pregnancy

 When there is severe ischemia, a portion of the kidneys' cortex becomes entirely necrotic, a condition known as acute cortical necrosis (ACN).  Because non-pregnant people's compensatory mechanisms are more active, ACN is more common in pregnant people than in non-pregnant people.

Any source of hypovolemia during pregnancy can produce ischemia and ACN directly because there aren't any functional compensating mechanisms in place.Septic abortion used to be the most frequent cause of ACN, although these days it is rare. Sepsis, antepartum hemorrhage, and preeclampsia are often observed causes.

Ten to twenty-five percent of cases of ACN result in irreversible loss of renal function.  Severe prenatal bleeding may cause ACN and complicate a healthy pregnancy and delivery, necessitating dialysis and possibly irreversible renal failure.

Natural History and Treatment of Acute Cortical Necrosis

The range of maternal mortality rates is 6–30%.  The fetus suffers negative consequences;  The course of treatment is cause-specific.

Threshold for Dialysis in Pregnancy and Modality Selection      

 Because high urea levels during pregnancy might harm the developing child by causing growth restriction, polyamnios, preeclampsia, and volume overload, the threshold for dialysis is low during pregnancy.  Unlike in non-pregnant situations, where larger levels may be tolerated, dialysis should begin if the BUN (blood urea nitrogen) level rises over 42.

Although there are no particular restrictions for peritoneal dialysis (PD) during pregnancy, hemodialysis (HD) is typically recommended due to the increased control over electrolytes and volume.

Although PD is safe in theory, there is a higher chance of peritonitis, which might hasten labor. While PD can result in issues related to the peritoneum, HD can affect uteroplacental perfusion because of abrupt fluid shifts.

Ovarian Hyperstimulation Syndrome (OHSS)

OHSS can result in AKI because of increased capillary permeability; it is caused by an excessive response to ovulation inducement during infertility treatment.  OHSS happens 3–7 days after delivering HCG. • The GnRH analog used to induce pregnancy causes follicular luteinization and the production of inflammatory mediators that raise capillary permeability and cause third spacing, haemoconcentration, and thrombosis risk.

Multiple stimulated follicles are indicative of OHSS, which can be diagnosed by blood study and USG.  IV fluids are used to manage third spacing and heparin is used to avoid thrombus formation owing to haemoconcentration. OHSS is normally self-resolving and resolves after 70 days in non-pregnant women and 10–20 days in pregnant women.

High-Yield Points

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