N 340 Women's Health & Illness in The Expanding Family & N345 Clinical Practicum

Readings: Chapters 18, 28 (pp 680-687), & 33

Review: ATI: Chapters 12 (pharmacologic pain management), 15 and 16.

1. What is chorioamnionitis and how are associated complications prevented?
1. What is dystocia and what are some causes?
2. When do hypertonic uterine contractions occur?
3. What interventions can be done for this abnormal labor pattern?
4. When do hypotonic uterine contractions occur?
5. What interventions can be done for this abnormal labor pattern?
8. What is precipitous labor? Being in labor for a short period of time sounds great, but what are some of the “down sides”?
6. What are some examples of pelvic dystocia?
7. What are some examples of soft-tissue dystocia?
9. What is CPD? What are some causes of CPD?
10. What’s back labor and why does it hurt so much?
11. What is the definition of prolonged labor?
12. What is the relationship between anxiety and prolonged labor?
13. Name two non-pharmacologic, two pharmacologic and two mechanical methods used to induce labor.
14. What’s a bishop’s score used for? What would be a “good” score?
15. What are prostaglandins (i.e. Cervidil, Cytotec) used for? What would be a contraindication for its use?
16. Amniotomies are very common in labor. For what purpose is an amniotomy used?
17. What are some side effects of oxytocin?
18. What are some ways to combat the effect of these side effects?
19. Generally, how is oxytocin administered ?
20. How is augmentation different from induction?
21. What are some nursing responsibilities with uterine forceps?
22. How about nursing responsibilities with a vacuum extraction?
23. Review the information on c-sections. It should sound very similar/familiar to abdominal surgeries you learned about last year. What might be some differences?
24. What’s a VBAC?
25. What are a couple of the major problems (one for the mother, one for the baby) of posterm labor?
26. What is so scary about shoulder dystocia?
27. What’s the problem with a prolapsed cord? What is the solution?
28. What maternal factors increased the likelihood of the very rare, but usually fatal AFE or ASP?

Chapter 18 Just know the basics.Cathy Clark and Karen Clark do a great job with specific examples during your clinical rotation. Look at 18-1 on pg 416. Review: ATI: Chapter 13.

1.What are some characteristics of a reassuring FHR pattern? Think about normal FHR, variability, accelerations and decelerations.

2. What are some characteristics of a non-reassuring FHR pattern (I bet you knew this question was coming!)? Think about normal FHR, variability, accelerations and decelerations. I find the figures on pp. 420-426 helpful. Don’t get caught up in the specifics. Read them with the intention of understanding the basic physiologic processes going on in that fetus (your other patient!)
3. What are some differences between internal and external monitoring (think about advantages and disadvantages of both).
4. What’s variability?
5. What things can affect variability?
6. What’s an early deceleration, what causes it and what would you do about it?
7. What’s a late deceleration, what causes it and what would you do about it?
8. What’s a variable deceleration, what causes it and what would you do about it?
9. What would be some advantages of fetal oxygen saturation monitoring for assessing fetal well being? How about fetal scalp sampling (p. 429)?
10. What’s an amnioinfusion used for?
11. What are some advantages of open glottis pushing as opposed to the valsalva maneuver (P. 464)?

Chapter 28 (pp 680-687), Placentas!!

1. What are the different types of placenta previas (figure 28-8)? What’s the worst kind to have?
2. What are the signs and symptoms of a placenta previa?
3. What kinds of abruptions are there (figure 28-10) and how are they graded? What are the symptoms of the three grades of abruptions?
4. What’s so serious about DIC? Check out pg 685 and box 28-2 on p. 686 and p. 737. (see below)
5. On p. 826: What’s the problem with a retained placenta?
6. Would you rather have a placenta accreta, increta or percreta (also page 826)? I remember which is which because they are in alphabetical order!

Jeanette Koshar's "Cheat sheet" on DIC (Disseminated Intravascular Coagulation)

 Diagnosis:

Underlying serious illness: sepsis, (usually gram-negative bacteria. Can be widespread bacterial or fungal though), severe tissue trauma (i.e. burns, head injury), ob complications (amniotic fluid embolus, abruptions, septic abortion, fetal demise, HELLP), shock, severe hypoxia, acidosis, autoimmune reactions (acute pancreatitis, graft rejections, anaphylaxis), cancer (esp. leukemia) and hemolytic transfusion reactions. They all damage the vascular endothelium. 50% related to ob problems, 35% with cancer and 15% for all other causes.

Hypofibrinogenemia, thrombocytopenia, fibrin degradation products (D-dimer) and prolonged prothrombin time.

Prolonged microangiopathic hemolytic anemia may be present

Physiologic response: Coagulation is initiated by underlying cause. Coagulation usually stays localized by blood flow and circulating coagulation inhibitors (antithrombin III). However if the stimulus to coagulation becomes too great, the demand on anticoagulants becomes too great. This cascade of events results in too much circulating thrombin which triggers the cleaving of fibrinogen, stimulation of platelet aggregation, activation of clotting factors V and VIII and the generation of plasmin (formed in a clot to slowly dissolve the clot). This plasmin then further cleaves fibrin. This time though that process results in fibrin degradation products, inactivates factors V and VIII resulting in hypofibrinogenemia, thrombocytopenia, depletion of coagulation factors and fibrinolysis.

Signs: Acute:digital ischemia and gangrene (too much thrombin) and spontaneous bleeding commonly from wounds and venipuncture sites. Subacute: (mostly seen with leukemia or other cancers): recurrent superficial and deep vein thrombosis. Since fibrin degradation products are cleared by the liver, liver dysfunction can occur resulting in abnormal liver enzymes. Obviously then, liver dysfunction can me the situation worse. Labs: Hypofibrinogenemia is a classic lab finding as is falling fibrinogen (<200 with <50 being critical) levels.

Other abn labs values: elevated fibrin degradation products, thrombocytopenia (platelets < 150), prolonged prothrombin time (> 30 seconds).

Prolonged: PT, PTT, bleeding time and thrombin time.

Decreased: fibrinogen, platelet count, clotting factors II, V, VIII and X and antithrombin III.

Increased: Fibrinopeptide A and fibrinolysin test

Positive: Fibrin split products and D-dimer (a fibrin degradation product that denotes action on cross-linked fibrin, not just plasmin on unclotted fibrinogen).

Chest x-ray: may have interstitial edema defuse microemboli in the lungs.

Elevated BUN and creatinine if severe hypovolemia and/or thrombi in the renal vasculature.

Physical exam:

Mental status: alterations in LOC and seizures esp with hypovolemia, cerebral hemorrhage or thrombosis.

Respiratory: may have tacypnea. Pulmonary secretion may be bloody. May hear crackles if microemboli.

Cardiac: dysrhythmias, hypotension, pulses weak and thready.

Urinary track: hematuria, oligouria,

GI: Hematemesis, occult blood. BS may be hyper (GI bleed) or hypo (hypovolemia)

Skin: diaphoretic, petechiae, ecchymoses (these may be 1st signs), hematomas, cyanosis, acrocyanosis, pallor, jaundice (if microcalcifications in liver), Epistaxis.

Treatment:

Nursing responsibilities: Know who is at risk, sophisticated assessment skills, interpreting lab values, assess response to therapy. Handle patient gently. Immobility precautions, pain assessment, nutritional support, patient anxiety and fear, support of family:

Underlying disorder needs to be treated. If clinical manifestations of DIC are mild this may be all that is needed.

Replacement therapy: platelets (to keep platelets above 50), cryoprecipitate (to replace fibrinogen to at least 150. One unit of c. will raise fibrinogen 6-8 mg/dL),

Heparin (paradoxical, but true). Controversial. Won’t be used it pt to undergo a neurosurgical procedure). Used in combination with replacement therapy. Dose: 500-750 units/hr. However antithrombin III levels must be >50% for heparin to work. Fresh frozen plasma is used to raise the level.

Looking for: rising fibrinogen level and a decline in fibrin degradation products (d-dimer) over 1-2 days. Also platelets should rise, but that takes at least a week.

If bleeding is still not controlled: aminocaproic acid (1 gm Iv/hr) or tranexamic acid (10 mg/kg q. 8 hrs. is added to heparin to increase blood clotting.

Differential Diagnoses:

Liver disease: can have prolonged PT and PTT, but fibrinogen and platelet counts are usually nl or close to it. Severe liver disease can be trickier.

Vit K deficiency: will have nl platelet count and fibrinogen level.

Sepsis: low platelets and digital ischemia may be present, but fibrinogen level should be nl.

References: Tierney. Current Medical Diagnosis and Treatment.

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