Postpartum haemorrhrage

Postpartum haemorrhrage

Primary PPH is defined as blood loss of greater than 500 mL within 24 hours of delivery and affects about 5% of deliveries.

There are many known risk factors: prolonged third stage pf labor, preeclampsia, multiple gestation, foeceps delivery, and mediolateral episiotomy.

The three most common causes of PPH are uterine atony, retained placenta, and cervical/vaginal lacerations.

Retained placenta

This is the second most important etiology of PPH (roughly 20%–30% of cases).

It is suggested by the finding of an absent or incomplete placenta. If delivery of the placenta has not taken place, it must lead without delay to manual removal of the placenta, under anesthesia whenever possible, to ensure uterus emptying.

Uterine atony

Uterine atony is the leading cause of PPH, observed alone in 50% to 60% of cases; it presents as painless continuous bleeding, often developing slowly at the beginning.

 The other key diagnostic criterion is abdominal palpation of a soft and oversized uterus.

Prevention relies on active management of the third stage of labor.

Treatment is based on bladder emptying and oxytocin (10–20 IU; ±uterine massage). When these measures are not quickly effective cervical/vaginal lacerations must be searched for and then be followed by rapid implementation of prostaglandin treatment if bleeding still persists.

Cervical/vaginal lacerations

This is the third cause of PPH (roughly 10% of cases), and it is more likely to occur after instrumental extraction, fetal macrosomia, or quick labor and delivery before full cervical dilation.

Diagnosis is also suggested when retained placenta and uterine atony have been discarded. this diagnosis is often made much too late (the bleeding can be concealed in the vaginal wall or pelvis), when the parturient displays hemodynamic instability, coagulation disorders, and increasing pelvic pain.

Uterine inversion

This is a rare iatrogenic event (!1/1000) where the internal surface of the uterus is partially or completely exteriorized into the vagina. Clinical features include abdominal pain and often severe hemodynamic instability.

Immediate uterine reversion must be performed by the obstetrician and can be facilitated by short-time tocolysis (trinitrine as first line), using usually a potent IV vasopressor at the same time to counteract hypotension (phenylephrine or adrenaline).

Coagulation disorders

Coagulation disorders can be the cause or the consequence of PPH. Many causes can be listed (congenital, such as von Willebrand disease, or acquired,

such as HELLP syndrome, disseminated intravascular coagulopathy, anticoagulation therapy, etc). In fact, coagulation disorders are rarely a true triggering

cause of PPH.

Planning for obstetric hemorrhaged organizational aspects

The effective management of obstetric hemorrhage relies on very simple but often overlooked principles that all concur to timely treatment:

_ Simultaneous, coordinated, multidisciplinary management (ie, obstetricians, anesthesiologists, hematologists, laboratory and blood bank technicians, radiologists).

_ Consensual and practical definition of hemorrhage: any abnormal bleeding (in rate or duration) should trigger at once the diagnosis ofhemorrhage. This is particularly important after delivery where the border between physiologic bleeding and PPH must be clear-cut to avoid

any treatment delay.

_ Consensual, preplanned, step management available as a written operational protocol.

_ As a first step, the obstetric team needs to focus on the search and basic treatment of the three most common causes of PPH: retained placenta

(manual removal of the placenta and manual uterine exploration), uterine atony (bladder emptying and IV oxytocin _ uterine massage), and cervical/vaginal lacerations (examination of the vagina and cervix with

appropriate valves, and repair as needed). Simultaneously, the anesthetic team provides basic resuscitation and adequate analgesia for these obstetric interventions.

_ The second step is implemented as soon as the first step has proven ineffective at stopping the bleeding and no later than 30 minutes after initial PPH diagnosis, to improve effectiveness. It mainly relies on prostaglandin administration, either IV prostaglandin E2 (PGE2)

sulprostone or intramuscular 15-Methyl prostaglandin F2a

(PGF2a) carboprost; uterine tamponade can also be useful. More advanced resuscitation and monitoring are also usually needed and provided by the anesthetic team at this stage.

_ The third step is considered within an additional 30 minutes (and no longer than after 1 hour) if the second step has also failed to stop bleeding. It relies on invasive therapy, either surgical artery ligation _ B-lynch suture or

radiologic embolization.

_ The last step is hysterectomy; meanwhile, the use of recombinant activated factor VII (rFVIIa) can be considered.

Invasive therapy

Several invasive options are available to control PPH when medical treatment is unsuccessful at controlling bleeding: uterine balloon tamponade, arterial embolization, uterine compression sutures, and internal iliac artery ligation.

Uterine balloon tamponade

Uterine packing has long been the treatment of choice to manage PPH; it is safe, quick, and effective in a majority of cases. Various balloon devices have been used, with the Sengstaken-Blakemore esophageal catheter being the most frequently employed.

Uterine arterial embolization

Another less radical approach to control bleeding is the use of uterine artery embolization. It has become a well-recognized alternative method of treatment in the conservative management of PPH in association with

local or medical treatment, or in the event of their failure.

The reported success rate

of uterine artery embolization in the literature is more than 90%.

In most patients, fertility is preserved and normal menstruation returns almost 100%. Minor complications such as pain and transient inflammation with fever are rare (0%–10%). More severe complications such as

pelvic infection, pulmonary embolism, or uterus and bladder necrosis have been reported.

B-Lynch suture

the so-called B-Lynch uterine compression suture has been used successfully to control bleeding following failed conservative management.

This technique also allows uterus conservation for subsequent menstrual function and pregnancies and seems to be devoid of long-term sequelae.

Surgical iliac (or uterine) artery ligation

When uterine tamponade and arterial embolization fail, a laparotomy to perform iliac artery ligation is an option to preserve the uterus. It can also be performed as a first invasive option, during C-section delivery, or when

the patient is hemodynamically unstable or if embolization is not readily available.

When arterial ligation fails, hysterectomy is usually necessary. This may carry a higher risk of morbidity when compared with emergency hysterectomy performed

Without prior iliac artery ligation.

Hysterectomy

As a last resort, but decided on quickly when all other interventions have failed, peripartum emergency hysterectomy may be required to control bleeding and save lives.

Transfusion therapy and resuscitation

Transfusion should be initiated with red blood cells in all obstetric patients with signs of inadequate oxygen carrying capacity and inmost obstetric patients with a hemoglobin of less than 7 g/dL, or when blood loss is ongoing and the hemoglobin is around 7 g/dL. If

hemorrhage is accompanied by coagulation disorders, 15 to 20 mL/kg of fresh frozen plasma should be given as first-line treatment and target hemoglobin should be set higher, above 8 g/dL, to improve overall coagulation activity. Transfusion of platelet concentrates is recommended to treat active bleeding associated with thrombocytopenia below 50 G_L_1

Intraoperative cell salvage

Intraoperative cell salvage (or preoperative autologous donation in scheduled cases) has an undisputed role in obstetrics in patients with high risk such as placenta previa/accreta, massive fibroids, or rare blood type

or unusual antibodies. Intraoperative cell salvage can be also useful in the treatment of Jehovah’s Witnesses or in geographic areas where allogeneic blood supply is particularly problematic.

Recombinant factor VIIA (NovoSeven)

It was suggested that rFVIIa was often effective at

stopping or reducing the bleeding, particularly when other conventional treatments (see above) had failed. The dosage used varied roughly from 20 to 120 mcg/kg, without clear evidence of a dose-response relationship.

Nonetheless, because of lack of level 1 evidence, the use, dosage, and timing of rFVIIa are still a matter of debate.

‘‘rFVIIa may be considered as treatment for life-threatening post-partum hemorrhage, but should not be

considered as a substitute for, nor should it delay, the performance of a life-saving procedure such as embolization or surgery, nor the transfer to

a referring center.

Continuous Femoral Nerve Block

Single Injection Femoral Nerve Block

FEMORAL NERVE BLOCK

 
 FEMORAL NERVE BLOCK

Historically this block was also known as the “3-in-1

block,” suggesting that the femoral, lateral femoral

cutaneous, and obturator nerves could be blocked

from a single paravascular injection at the femoral

crease. Studies have since demonstrated that the

femoral and lateral femoral cutaneous nerves

can be reliably blocked by a single injection, but

the obturator nerve is often missed. Therefore, a

posterior lumbar plexus block should be used when

all three nerves need to be anesthetized (although

this point remains controversial). The femoral

nerve block is an ideal block for surgeries of the

hip, knee, or anterior thigh and is often combined

with a sciatic nerve block for near complete lower

analgesia. Complete analgesia of the leg

can be achieved without lumbar plexus block by

extremity

combining a femoral nerve block with parasacral

sciatic nerve block (which blocks the obturator

over 90% of the time), or by adding an individual

obturator nerve block to the femoral nerve block.

ANATOMY

The femoral nerve, formed by the dorsal

divisions of the anterior rami of L2–L4, is the largest

terminal branch of the lumbar plexus. It travels

through the psoas muscle, leaving the psoas at its

lateral border. The nerve then descends caudally

into the thigh via the groove formed by the psoas

and iliacus muscles, entering the thigh beneath the

inguinal ligament . After emerging

from the ligament, the femoral nerve divides into

an anterior and posterior branch. At this level it is

located lateral and posterior to the femoral artery

. The anterior branch provides motor

innervation to the sartorius and pectineus muscles

and sensory innervation to the skin of the anterior

and medial thigh. The posterior branch provides

motor innervation to the quadriceps muscle (rectus

femoris, vastus intermedius, vastus lateralis, and

vastus medialis) and sensory innervation to the

medial aspect of the lower leg via the saphenous

nerve.

The anatomic location of the femoral nerve makes

this block one of the easiest to master because the

landmarks are usually simply identified (except in

cases of morbid obesity), the patient remains supine,

and the depth of the nerve is relatively superficial.

PROCEDURE

Landmarks.

anterior superior iliac spine and the pubic symphy

and draw a line between these two landmarks.

This line represents the inguinal ligament. The

Place the patient supine, identify thesis,

femoral nerve passes through the center of the line,

which makes this landmark useful for positioning

the needle in the inguinal crease, particularly in an

obese patient. Then palpate the femoral pulse and

mark it at the inguinal crease. Studies have dem

that the most successful point of needle

onstrated

entry is directly lateral (1–1.5 cm) to the artery in the

inguinal crease. At this location the femoral nerve is

wide and superficial, and the needle does not pass

through significant muscle mass. Direct the needle

cephalad toward the center of the inguinal ligament

line.

Needles

• 22-gauge, 5-cm insulated needle.

• 18-gauge, 5-cm insulated Tuohy needle for

catheter placement. The catheter is inserted 3 to 5

cm for the femoral block.

Stimulation.

The nerve stimulator is initially set

at 1.0 to 1.2 mA. The needle is directed cephalad at

approximately a 30° to 45° angle. A brisk “patellar

snap” with the current at 0.5 mA or less is indica

of successful localization of the needle near

tive

the femoral nerve. The nerve is usually superficial,

rarely beyond 3 cm from the skin .

Local Anesthetic.

In most adults, 20 to 40 mL of

local anesthetic will produce a successful femoral

block.

Teaching Points.

Studies have demonstrated

that the anterior branch of the femoral nerve is

usually encountered with the first needle pass,

which results in stimulation of the sartorius

muscle, often seen as contraction of the lower

medial thigh. If this occurs, advance the needle

tip until either the sartorius twitch is extin

or a patellar snap is elicited before redi

the needle. If the sartorious twitch is ex

without the patellar snap, withdraw

guishedrectingtinguished

the needle toward the skin (without exiting

the skin), and redirect it slightly lateral and

slightly deeper than the original needle pass.

The posterior branch of the femoral nerve is

typically lateral and deep to the anterior branch.

The anesthetist should resist the urge to use

the patient’s thigh as a hand rest while directing

the needle. Stimulation of the femoral nerve can

result in brisk vastus muscle twitching that can

disrupt needle positioning.

The femoral nerve block provides analgesia to

the anterior thigh, including the flexor muscles

of the hip and extensor muscles of the knee.

Spirometry

Spirometry: how to take a lung function test

Pulmonary Function Tests (About The Respiratory System)

Pulmonary Function Tests (About The Respiratory System)

Pulmonary Function Tests

What are pulmonary function tests?

Pulmonary function tests are the main tool that pulmonologists use to diagnose pulmonary diseases and they are easily accomplished tests. Sometimes it's done in the primary care physician's office in what we call a very simple spirometry or a blow and go, where you take a deep breath, blow into a machine, and go, but the pulmonary function studies done by a pulmonologist in a pulmonary function lab take about an hour. They require the patient to be able to sit and breathe at different rates, take deep breaths, and blow them out as fast as possible. That generates an enormous amount of information about the different compartments in the lung, we look at all that data then we can say "This patient has primarily an obstructive lung disease and this is where the obstruction occurs, small airways, large airways or he has a restrictive lung disease which would be an interstitial lung disease" and the data tells us a lot of information about severity, prognosis, and gives us an opportunity to tailor make therapy for the patient.

What is a "spirometer"?

A spirometer is a device that allows for you to take a deep breath, blow into; then it calculates, stores the data on how fast the patient was blowing, what the volumes are that they're blowing; and it allows then for this information to be fed into a computer. And the current spirometers are very accurate and very easily operated and give us a tremendous amount of information.

How is a spirometry testing performed?

A spirometry test requires a patient to arrive at the testing site, be prepared to sit for about an hour, take a deep breath and blow into the machine. The respiratory therapist that will administer the test will be very good at coaxing the patient step-by-step through the test and informing them how they want that test to be performed. The therapist will be looking for what is called a "flow volume curve" during the spirometry test. So, when the person inhales, the inspatory lube and expiatory lube, is noted against flow and volume and then the speed with which the person can exhale is also noted. For instance, in patients with asthma, do the airways collapse as they start to exhale? What happens when they inhale? We can tell whether or not the obstruction is in the upper airways or the lower airways, by the shape of the curve during the spirometry test. We can then see what happens if a person inhales a bronchial dilator. We can discover if their airway opens up and responds nicely to the application of the bronchial dilator and once again we can disvoer how that patient's lung is reacting to their particular problem with their lung.

How will spirometry feel?

Spirometry will feel painless for the most part. Some patients object to it because they don't like the period where they have to take deep breaths and blow it out and take another deep breath and blow it out. They sometimes have to huff and puff a bit, and they'll complain about that. But for the most part, patients who have had spirometry will tell you that it was really no problem, and it was just a matter of being coaxed by the respiratory therapist, and it shouldn't be uncomfortable at all.

What is a "peak flow" meter?

A peak flow meter is really a dandy little device. I pass out peak flow meters to patients constantly. It's a little plastic gadget that they can take home with them, and they open it up and unfold it and it has a little slider on it. It reminds me of going to the fair ground, where you take a hammer and you pound it down and the ball goes up has high as it can go based on how hard you hit the device at the bottom that will eject the device up the scale. Well, a peak flow meter requires you to take a deep breath and you punch it, and you want to get the peak flow, the fastest you can, to run the slider up as far as it will go. These devices are simple, they are cheap, but they will give you a enormous amount of data. This is especially the case with asthmatics, where the data from taking a peak flow meter reading will tell you that you're about to get an attack of asthma. It can be predictive of an oncoming attack, so you can increase your medications as you need to. What we try and do is get the patient to develop their personal best. That term means how far they can push that little slider up when they take a deep breath, and they exhale forcefully into it. It's not a matter of how long you inhale, its that first punch and you really get it. You want to bounce that thing as far down the scale as you possibly can. Then, you set some limits back from that, which will tell you whether you're starting to have an attack or not. It's a very, very nice, cheap inexpensive way to do home pulmonary function testing.

Why would my doctor order peak flow testing?

Most of us pulmonologists will order peak flow testing because we want the asthmatic patients, primarily, to keep a day by day, if not twice a day, log of what their treatment is doing to their airflows and how they're responding to their environment with their asthma. So, I'll order a peak flow test not as a single test, but I'll ask them to do it on a daily basis to help them understand how well their medications are doing and number two, whether or not they're developing an asthma attack and they need to be positioned in such a way that they get better control, maybe in escalation of their medicines, somewhat, so they'll have better control over their airways. If you're an asthmatic and using peak flow properly, you'll know that your peak flow personal best may be 400 liters per minute flow. If you suddenly see that you, for the next 12 hours, drop your flow rates down to, let's say 300 or 250, you pretty well can bet that you're on your way to having a major attack. Therefore, you should increase your medications, or let's say that it would go to 200, which is fifty percent of your personal best at 400. With 200, you should pick up your phone and say "Can I have an appointment tomorrow morning with my pulmonologist?", or you might decide it's time for you to go to the emergency room. Because, certainly if your personal best is 400 and you're down to 200 you will be very short of breath and you will be very uncomfortable.

What is a "diffusion capacity lung" test or "DCLO" test?

A diffusion capacity lung test is a specialized test that helps us understand the health of the alveolar-capillary membrane. Now remember that the alveolus is a thin membrane that allows for oxygen and CO2 to move across this membrane. Well this membrane is tested best by the diffusion capacity, and there are several ways of doing diffusion capacity but they all require that you inhale a minute amount of carbon monoxide. Carbon monoxide moves across the alveolar-capillary membrane in such a way that it is not blocked at all by, it's not blocked at all by its diffusion ability. It is rapidly absorbed across the membrane into the red blood cells, but if that membrane becomes diseased it will in some way then limit the ability of the carbon monoxide to move, to move across. So that the only thing that is a variable there is the state of health of the alveolar-capillary membrane. Now, if in, like, for instance, emphysema, emphysema is a disease where these alveoli fuse together. Where you used to have one aveloli you now have--you used to have two, you now have one. The surface area of two alveoli is greater than the surface area of one when you combine those two together, and so you'll start to lose diffusion capacity because the surface area is being lost, and that's what emphysema does--one of the many things it does--to damage your lung. So diffusion capacities will help you not only help you establish the health of the alveolar-capillary membrane using the inhalation of carbon dioxide--not enough to poison you of course, but just minute amounts--and it'll also tell you about the size of your alveolar-capillary membrane as an aggregate whole. Are you losing surface area? We lose surface area as we age naturally, however, we'll not lose it as fast as if you are a significant smoker who then develops emphysema and then start to lose surface area, and that'll be picked up by diffusion capacity.

Why do I need a DCLO or diffusion capacity lung test?

The reason for taking a diffusion capacity test would be to help you establish the health of the alveolar-capillary membrane. The standard pulmonary function test in almost all pulmonary function labs that a pulmonologist will run, or order tests to be performed at, includes diffusion capacity in the test. If you are getting your test done simply in a primary care physician's or a general practitioner's office, he won't have the machinery available to him and the testing devices available to him to do a diffusion capacity. But if a full pulmonary function test is done, diffusion capacity is part of that test, always.

How is a DCLO or diffusion capacity test performed?

The diffusion capacity test is performed in several ways, depending on how you're set up to do it. There's really three different ways of doing it. There's the single breath method where you take a deep breath and hold it for ten seconds. There's also a rebreathing technique, where you rebreathe the carbon monoxide. There's a steady state test, where you keep breathing it until you reach what's called "steady state." All of which are quite painless, quite easily performed, and it will depend a lot on the lab and the type of patient you have whether you do a steady state, single breath, or a rebreathing form of the diffusion capacity test.

How will a DCLO test feel?

When people take a diffusion capacity test as part of their pulmonary fuction test, they really don't feel anything. They don't feel the gas, they don't taste the gas, it doesn't make them dizzy, it doesn't do anything that would be noxious. If they have trouble holding their breath for ten seconds they may find that to be uncomfortable, but by and large there's nothing to feel.

What do abnormal DCLO results mean?

An abnormal result on a diffusion capacity could mean several things. It could mean that you've lost surface area, such as would be encountered in patients with emphysema. It could also mean that the health of the alveolar capillary membrane has been diminished and so you have a damaged alveolar capillary membrane. It may be the very first thing that you would pick up in interstitial lung diseases. Where every thing else is normal, one of the earliest findings in some of the interstitial lung diseases such as, for instance, sarcoi, would be an abnormal diffusion capacity.

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