lumen of most dairy cattle in the first two weeks after parturition in many situations, although
in some countries the frequency is lower [2-6]. Although many cows eliminate these bacteria
during the five weeks after parturition, in 10 to 17 % of animals persistence of bacterial infection
causes uterine disease clinically detectable by physical examination [7,8]. The presence of
bacteria in the uterus causes inflammation, histological lesions of the endometrium, delays
uterine involution and perturbs embryo survival [9-11]. In addition, uterine bacterial infection,
bacterial products or the associated inflammation suppress pituitary LH secretion, and perturbs
post partum ovarian follicular growth and function, which disrupts ovulation in cattle [5,
12-14]. Thus, uterine disease is associated with lower conception rates, increased intervals
from calving to first service or conception, and more culls for failure to conceive [7,8,15,16].
The goal of bovine reproduction management is to have cows become pregnant at a biologically
optimum time and at an economically profitable interval after calving. The timing of
examination of animals after parturition should allow for the normal process of involution, yet
also provide time for treatment and response prior to the start of the breeding period. The aims
of uterine disease treatments are to reverse inflammatory changes that impair fertility, whilst
enhancing the processes of uterine defence and repair.
As bovine uterine disease is so important, it is not surprising that more than 500 papers have
been published in the last 40 years on the most common uterine diseases, metritis, endometritis
and pyometra [17]. Indeed, there are several review articles with extensive citation lists [1,
18-23]. However, frequently the definition or characterization of the various manifestations of
uterine disease either lack precision or definitions vary between research groups and/or were
not validated as to their effect on reproductive performance, making assessment of the effects
of treatment difficult [24]. Often the term endometritis incorrectly includes metritis,
endometritis and pyometra, and/or is determined solely on the basis of transrectal palpation of
an enlarged uterus [25,26]. During the 15th International Congress on Animal Reproduction
(2004) it was suggested that the research field would be aided by clear definitions of uterine
disease that researchers could adopt. Thus, in the present paper we outline the key clinical
features of uterine disease in cattle and suggest working definitions to reflect the character of
these diseases.2. Uterine bacterial contamination and infection
The majority of post partum inflammatory conditions of the uterus begin with bacterial
contamination of the uterine lumen. One should differentiate between uterine
contamination and uterine infection . The uterus of post partum cows is usually contaminated
with a range of bacteria, but this is not consistently associated with clinical disease. Infection
implies adherence of pathogenic organisms to the mucosa, colonization or penetration of the
epithelium, and/or release of bacterial to xins that lead to establishment of uterine disease
[27]. The development of uterine disease depends on the immune response of the cow, as well
as the species and number (load or challenge) of bacteria. The number of pathogenic bacteria
in the uterus of post partum cows may be great enough to overwhelm uterine defense
mechanisms and cause life-threatening infections, although these are relatively uncommon
[1]. Indeed, it is non-life-threatening uterine infections that are most common and associated
with impaired reproductive performance [8]. Furthermore, inflammation even in the absence
of active bacterial infection, may perturb embryo survival [28,29].
Establishment of uterine bacterial infection may depend in part on the endocrine environment
and in particular progesterone seems to suppress uterine immune defences. Formation of the
first post partum corpus luteum and secretion of progesterone precedes the onset of many
uterine infections [21,30]. Indeed, intrauterine infusions of Arcanobacterium pyogenes and
Escherichia coli into post partum beef cows under experimental conditions did not establish
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infections, unless peripheral plasma progesterone concentrations had started to increase [31].
However, many spontaneous uterine infections are established within 3 wk of parturition,
before ovulation of the first dominant follicle [5,32]. Furthermore, chronic uterine infection
and increased plasma concentrations of lipopolysaccharide (LPS) are associated with
disruption of the LH surge and failure of ovulation [1,14,33]. The relationship between uterine
bacteria, the immune or inflammatory response, and ovarian function are complex and require
more investigation, although it appears that uterine disease is associated with anovulatory
anestrus and cystic ovarian disease [12,34]. On the other hand, the immunosuppressive effects
of progesterone from the corpus luteum, or possibly adrenal steroids, may contribute to the
progression of uterine contamination into uterine infections. The mechanisms of action of
progesterone are complex, not completely understood, and not within the scope of this article.
However, the knowledge that progesterone is immunosuppressive at a number of levels and is
involved in regulating the synthesis of prostaglandin F 2α (PGF 2α), plus a variety of
immuomodulatory cytokines, can be useful for managing uterine infections. In cows with a
functional corpus luteum, administration of exogenous PGF 2α is used to stimulate luteolysis,
reduce progesterone and increase oestrogen concentrations, induce estrus and resolve uterine
infections [21,35,36]. Estrus appears to be particularly beneficial to the resolution of uterine
infection [37]. Exogenous PGF 2α may enhance immune functions or increase uterine motility
to help the uterus resolve infections in animals that do not have active corpora lutea [38,39].
However, the results of clinical trials of PGF 2α for treatment of clinical endometritis in the
absence of an active corpus luteum are inconsistent [40-42]. Indeed, investigation by meta-
analysis of many studies reporting the effect of prostaglandin F2 alpha administered post
partum indicated little benefit to the reproductive performance of dairy cattle [43]. An
alternative effective treatment for endometritis is intrauterine infusion of antimicrobials [35,
40,42].
Involution of the genital tract after parturition also aids the resolution of uterine infection, and
conversely may be delayed by uterine disease. In addition, evaluating uterine and cervical
involution may help to differentiate between physiological and pathological observations. In
normal cattle, the cervix re-opens after a week post partum [44]; and lochia is passed until 15
to 20 d post partum and over the course of involution, lochia changes from a red-brown fluid
to a more viscous yellow-white material. Healthy cows achieve a uterine horn diameter of 3
to 4 cm by 25 to 30 d post partum, and cervical diameter < 5 cm by 40 d post partum, but
complete involution of the uterus and cervix takes until approximately 40 to 50 d post partum
[18,45]. However, uterine involution can also be affected by age, breed, nutrition and other
factors so that delayed uterine involution is not a specific indicator of uterine disease [46].
In summary, bacteria from the surface of the animal and the environment contaminate the
uterine lumen of most post partum cows. Elimination of this contamination is dependent on
uterine involution, regeneration of the endometrium, and uterine defense mechanisms. The
influx of polymorphonuclear neutrophils (PMN), attracted by chemokines such as interlukin-8
(IL-8), plays a key role in the uterine immune response [47]. However, ovarian activity and
luteal progesterone modulate many of the processes that make a cow resistant or susceptible
to uterine infections, and exogenous PGF 2α or intrauterine antimicrobials are effective
treatments.3. Pathology
To the pathologist the general definitions of inflammation of the genital tract are simple.
Inflammation limited to the endometrium is termed endometritis; involvement of the entire
thickness of the uterine wall is metritis; of the serosa, perimetritis; and of the suspensory
ligaments, parametritis [20,48]. Metritis can be distinguished from endometritis; in the former,
all layers of the uterine wall show evidence of inflammation such as edema, infiltration by
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leukocytes, and myometrial degeneration. In both conditions, the mucosa is congested, and
there is a prominent leukocyte infiltration in response to the common pathogens
Arcanobacterium pyogenes , Fusobacterium necrophorum , Prevotella species and Escherichia
coli . In particular, infection with A. pyogenes is associated with increased time to pregnancy
[16,49]. Endometritis is a superficial inflammation of the endometrium, extending no deeper
than the stratum spongiosum [20]; with histological evidence of inflammation (Fig 1(a) and
Fig 2(a)). During recovery from acute endometritis, there is fibrosis and leukocytosis, with
depletion of endometrial glands and atrophy of the remainder.
Pyometra is associated with corpus luteum activity in the ovary, often its persistence for greater
than the expected duration of the luteal phase. It has been suggested that it is the presence of
this structure with its secretion of progesterone that results in endometritis developing into
pyometra [48]. Early ovulation after parturition and formation of an active corpus luteum may
predispose to pyometra [50,51]. On the other hand, the retention of the corpus luteum may be
associated with failure of the luteolysin, prostaglandin F 2α to reach the ovary. The role of
progesterone may be to maintain functional closure of the cervix as well as increasing the
susceptibility to persistent infection, especially with A. pyogenes and anaerobic bacteria [51].4. Clinical definitions
Puerperal metritis is an acute systemic illness due to infection of the uterus with bacteria after
parturition. Puerperal metritis is characterized by the following clinical signs: a fetid red-brown
watery uterine discharge and, usually, pyrexia [52]; in severe cases, reduced milk yield,
dullness, inappetance or anorexia, elevated heart rate, and apparent dehydration may also be
present. The term metritis should be used for cows that have delayed involution and a fetid
discharge, in the absence of detected fever. Indeed, in some cases of severe bacterial infection
pyrexia was not detected even with daily monitoring of rectal temperature and did not depend
on the load or species of bacteria [53]. Puerperal metritis is often associated with retained
placenta, dystocia, stillbirth or twins and usually occurs toward the end of the first week post
partum, being rare after the second week post partum [52,54]. We propose that the definition
of clinical puerperal metritis in a cow should be characterized by overt systemic illness
(decreased milk yield, dullness or other signs of toxaemia) associated with a fetid watery red-
brown uterine discharge, often associated with fever > 39.5°C and an enlarged uterus. Animals
that are not ill, but have an enlarged uterus and a purulent uterine discharge may be classified
as having clinical metritis.
Clinical endometritis is characterised by the presence of purulent (> 50% pus) or
mucopurulent (approximately 50% pus, 50% mucus) uterine exudate in the vagina, 21 d or
more post partum, and is not accompanied by systemic signs [7,42]. Diagnostic criteria for
clinical endometritis in post partum dairy cows, have been validated by examining factors
associated with an increased time from parturition to conception [7]. The significant factors
were the presence of purulent vaginal mucus or a cervical diameter > 7.5 cm, 21 d or more
post partum; or, after 26 d post partum, the presence of a mucuopurulent material in the vagina.
Using this classification for endometritis, the incidence was 16.9 % for the 1865 cows
examined. The temporal differences in the significant factors probably reflect the progress of
uterine involution and immune defense. Classifying animals as having clinical endometritis if
they are < 21 d post partum may include a greater proportion of animals that are spontaneously
resolving bacterial contamination, and so reflect the presence of disease less accurately.
Furthermore, variations in appearance of normal lochia confound diagnosis of endometritis at
this stage. Similarly, using delayed involution alone to diagnose endometritis is unreliable, as
the enlarged uterus may reflect physical damage or variations associated with breed, age, or
nutrition rather than bacterial infection, whilst the small increase in diameter of the uterine
horns may be difficult to detect in mild cases of endometritis. Thus, although the pathology of
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interest involves the uterus, palpation of the uterus to asses its size lacks diagnostic accuracy
[7,55]. However, estimation of cervical diameter by palpation was associated with clinical
endometritis and appears to be a more reliable marker of delayed involution [7,56,57]. In
summary, we propose that the definition of clinical endometritis in a cow is the presence of
purulent uterine discharge detectable in the vagina 21 d or more post partum, or mucuopurulent
discharge detectable in the vagina after 26 d post partum.
Subclinical endometritis can be defined as endometrial inflammation of the uterus usually
determined by cytology, in the absence of signs of clinical endometritis [58]. In animals without
signs of clinical endometritis, subclinical disease was diagnosed by measuring the proportion
of neutrophils present in a sample collected by flushing the uterine lumen (Fig. 1(b) and Fig.
2(b)), or using a cytobrush [19,59,60]. Subclinical endometritis was determined by the presence
of > 18 % neutrophils in uterine cytology samples collected 20 to 33 d post partum or > 10 %
neutrophils at 34 to 47 d post partum, or by ultrasonic imaging of a small volume of mixed
echogenicity fluid within the uterine lumen, in the absence of abnormal mucus in the vagina
[60]. The incidence of clinical and subclinical endometritis was 53% at 40 to 60 d post partum,
and was associated with delayed conception and increased culling [61]. The assessment of
inflammation at 40–60 days post partum corresponded approximately to >5% neutrophils
[61]. Although investigation of subclinical endometritis is at an early stage, we have used
available data to suggest a working definition. We propose that a cow with subclinical
endometritis is defined by > 18 % neutrophils in uterine cytology samples collected 20 to 33
d post partum, or > 10 % neutrophils at 34 to 47 d, or by ultrasonic imaging of mixed
echogenicity fluid within the uterine lumen after 21 d post partum, in the absence of clinical
endometritis.
Pyometra is characterized by the accumulation of purulent or mucopurulent material within
the uterine lumen and distension of the uterus, in the presence of an active corpus luteum. There
is often an increased number of pathogenic bacteria within the uterine lumen when the corpus
luteum forms and pyometra occurs [51]. Although there is functional closure of the cervix, the
lumen is not always completely occluded and some pus may discharge through the cervix into
the vaginal lumen. Pyometra is sonographically characterised by a corpus luteum in an ovary,
accumulation of mixed echogenicity fluid in the uterine lumen and distension of the uterus. In
summary, we propose that pyometra is defined by the accumulation of purulent material within
the uterine lumen in the presence of a corpus luteum and a closed cervix.5. Diagnosis
It is important to be able to diagnose the presence of uterine infection to facilitate timely and
appropriate treatment and to quantify the severity of disease, which allows a prognosis to be
given for subsequent fertility. Unfortunately, there is no “gold standard” for diagnosis of uterine
disease, making it difficult to measure the sensitivity and specificity of clinical definitions. In
addition, there is little information on the correlation between clinical and histopathological
observations, although the presence of pus in the vagina is correlated with the presence of
pathogenic bacteria in the uterus [62,63]. The definitions we propose should allow
classification of disease in most animals, whilst accepting that clinical parameters may not
reflect the impact on economic or reproduction outcomes in all countries. Furthermore, there
is a continuum of peri-partum disease, so the consideration of what is abnormal and the
selection of cost-effective therapy will depend on the production system. Therapeutic cut-
points and decision trees would be useful for the different production systems.
The diagnosis of puerperal metritis is made readily from the clinical signs of illness and fetid
uterine discharge detectable on clinical examination. The diagnosis of pyometra depends on
transrectal palpation of a doughy, distended, thick walled uterus and/or transrectal
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ultrasonography of mixed echogenicity fluid, and the presence of a corpus luteum. The uterine lumen fluid of a pyometra can be displaced from one horn to the other, which cannot be done with fluids associated with a gravid uterus. The sensitivity, specificity and positive predictive value of palpation for identifying mid-cyclic corpora lutea were 85%, 95.7% and 89.5%,respectively, whilst for ultrasonography the values were 95%, 100% and 100%, respectively [64]. If necessary, progesterone concentration in milk or plasma can be measured to avoid a small proportion of animals being misclassified by errors in the physical detection of a corpus luteum.The definitive diagnosis of endometritis is made on the basis of histological examination of endometrial biopsies (Fig. 1(a) and Fig. 2(a)), and these are predictive for subsequent fertility [49]. However, the technique is costly and time consuming, and not clinically accessible in
most situations. Cytology is more practical (Fig. 1(b) and Fig. 2(b)) and is necessary to diagnose
subclinical endometritis [58,60]. However, neither of these procedures produces a rapid clinical
diagnosis. Thus, in the field, diagnosis of uterine disease usually relies on clinical examination.
Transrectal palpation for delayed involution is not a good technique for evaluating uterine
infection because it is subjective, uterine involution varies between cows, and there is little
association with reproductive performance [7,21]. In addition, although a marked delay of
uterine or cervical involution is associated with lower conception rates, it is the evaluation of
animals where the effects on uterine involution are less obvious that is more difficult. Similarly,
observation for abnormal vulval discharge is unreliable for diagnosis of endometritis [65]. The
use of clinical records of stillbirth, twins, retained fetal membranes, dystocia and hypocalcemia
helps identify animals at risk of uterine disease, but does not provide a specific diagnosis
[54,65,66]. Further examination of data from a large clinical trial confirms that disease history
alone lacks sensitivity for identifying cattle with clinical endometritis (Table 1). However, the
use of historical information may decrease the cost of diagnosis and hence increase the cost :
benefit of treatment for uterine disease for some farmers.
The use of transrectal ultrasonography permits more objective measurement of the diameter
of the uterine horns and cervix, and visualization of mucus and pus within the uterine lumen
[11,60,67]. At present, there is little evidence that ultrasonography provides more information
about clinical endometritis than examination of the contents of the vagina. Although, there is
limited information on the relationship between ultrasonographic findings and clinical or
subclinical endometritis, this is likely to be a fruitful area for research.
To diagnose clinical endometritis we advocate the examination of the contents of the vagina
for the presence of pus [7,22,42]. The simplest method is to perform a manual examination of
the vagina and withdraw the mucus for inspection [68]. The advantage of this technique is that
it is inexpensive, quick, provides additional sensory information such as detection of vaginal
lacerations and detection of the odor of the mucus in the vagina. One procedure is to clean the
vulva using a dry paper towel and insert a clean, lubricated gloved hand through the vulva into
the vagina. The lateral, dorsal and ventral walls of the vagina and the external cervical os are
palpated and the mucus contents of the vagina withdrawn for examination. The hand usually
remains in the vagina for less than 30 seconds. Manual vaginal examination has been validated
and does not cause uterine bacterial contamination, provoke an acute phase protein response,
or delay uterine involution [68]. However, the operator has to be aware that vaginitis or
cervicitis may give false results. Vaginoscopy can be performed using autoclavable plastic,
metal or disposable foil-lined cardboard vaginoscopes, which allow inspection of the contents
of the vagina. However, there may be some resistance to the use of vaginoscopes because of
the perceived inconvenience, potential for disease transmission and cost [7]. A new device for
examination of vaginal mucus (Metricheck?, Simcro, New Zealand) consists of a stainless
steel rod with a rubber hemisphere that is used to rake out the vaginal contents.
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Several scoring systems have been described to estimate the severity of clinical endometritis
[35,42,63]. The character of the vaginal mucus can be scored (Fig. 3) as well as odor (score 0
for no odor and 3 for a fetid odor) [63]. The character score reflects the presence and semi-
quantitative load of certain bacteria in the uterus. In one study [63], muco-purulent discharge
was associated with F. necrophorum and purulent discharge was associated with
Arcanobacterium pyogenes and Proteus species, whilst a fetid odor was associated with a
greater load of Arcanobacterium pyogenes , Escherichia coli , Streptococci , and Mannheimia
haemolytica . Clear mucus with flecks of pus was not associated with the presence of higher
numbers of pathogenic bacteria in the uterine lumen, but the effects on fertility are not
consistent [7,63]. These mild cases of endometritis may be resolving the uterine infection, and
the discriminators may not be sensitive enough to detect perturbation of reproduction.
However, subclinical endometritis is associated with lower conception rates to first service and
overall [19,60]. Thus, the absence of pus in the vagina does not always reflect the absence of
inflammation in the uterus.6. Conclusions
In conclusion, we have suggested clinical definitions for the common post partum uterine
diseases that can be readily adopted by researchers and veterinarians. Given the diagnostic
criteria that we present, it is possible to identify individual cows that are likely to have a
meaningful impairment of reproductive performance. A practical question is whether it is
economically beneficial to invest the time and resources necessary to find and treat cows with
endometritis. The optimum answer likely varies between farms, depending on the prevalence
of endometritis, the cost and accuracy of diagnosis, the efficacy and cost of treatment, the
pressure for early post partum breeding, and the use of systematic breeding programs including
prostaglandin F 2α for first insemination. Further research is needed to refine the inputs into
economic decision-making tools to answer these questions under a variety of management
conditions.
Acknowledgements
Supported by The Wellcome Trust and BBSRC (to IMS), USDA Animal Health and Disease Funds (to ROG).
We wish to thank the following people for kindly reviewing the manuscript, and contributing to this paper: Augustine
Peter, Doug Hammon, Ram Kasimanickam, Marc Drillich, Wolfgang Heuweiser, John Mee, Pat Hartigan, Aart de
Kruif, Gyula Huszinicza, Hans Kindahl, Robert BonDurrant, Richard Murray and David Noakes.
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Figure 1.
Photomicrographs from the same animal of (a) histological section of an endometrial biopsy
of normal tissue and (b) cytology of normal fluid collected by flushing the uterine lumen. Note
endometrial gland (arrow a) and blood vessel (arrow b) in histology. Cytology consists
predominantly of endometrial epithelial cells. Bar = 15 μm.
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Figure 2.
Photomicrographs from the same animal of (a) histological section of an endometrial biopsy
of inflamed tissue, with influx of polymorphonuclear neutrophils (arrow a), some slight
periglandular fibrosis (arrow b) and overall increased cell density due to cellular infiltration
(arrow c) and (b) cytiology of inflamed uterine fluid collected by flushing the uterine lumen,
with prominent polymorphonuclear neutrophils (arrows) amongst the epithelial cells. Bars =
15 μm.
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Figure 3.
Typical samples of vaginal mucus character score 0 = clear or translucent mucus; 1 = mucus
containing flecks of white or off-white pus; 2 = discharge containing ≤ 50% white or off-white
mucopurulent material; and 3 = discharge containing ≥ 50% purulent material, usually white
or yellow, but occasionally sanguineous [63].
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Table 1
The association of disease events in the first week post partum with diagnosis of clinical endometritis in the third and fourth weeks post partum. Although the prior diseases were strongly associated with the risk of clinical endometritis, over half the cows with endometritis did not have these risk factors.
Clinical Endometritis
Yes No Total
Had ≥ 1 of
twins, RP,
metritis
Yes73110183
No1229761098
Total19510861281
OR = 5.3, P < 0.0001
Sensitivity =37%, specificity = 90%
Data from LeBlanc et al (2002) and unpublished.
奶牛产后死亡的主要原因及治疗措施 分娩是母牛生产的关键时期，由于机体抵抗力下降，产道损伤和开放，暂时失去了自身的抗感染机能，极易受到外界病原微生物的感染。如没有及时有效地处理，局部的感染会波及全身，引起产后全身感染，发生败血症或脓毒血症。 病因： 主要来自难产、胎儿腐败、胎衣不下腐败分解，粗暴助产消毒不严、甚至不消毒，产道损伤严重等，外界大量病原微生物的侵入，引起严重感染。病原菌通常有溶血性链球菌、葡萄球菌、化脓性棒状杆菌等，并都为混合感染。 症状： 产后败血症体温上升至40-41℃，持续不降，呈稽留热型。四肢末梢发凉，精神极度沉郁，卧地呈半昏迷状态，食欲废绝，反刍停止，喜饮水。泌乳骤减，继而停止。脉搏速弱，达90-120次/min，呼吸浅快。随病程发展，患牛出现腹泻，粪中带血、腥臭，脱水，表现高度衰竭。 产后脓毒血症病情时好时坏，体温升高1-1.5℃，后又下降，甚至恢复正常，呈舒张热型，反应体内脓灶形成、局限，转移形成新脓灶的反复过程。脓灶可转移至四肢关节、肺、肝、肾、乳房等发生迁徙性脓肿，出现跛行，肺、肾及乳房等炎症的症状。 奶牛的败血症、脓毒血症，即使治愈，也会后遗泌乳下降和不孕，常以淘汰告终。 治疗： 本病病情发展急剧，必须及时治疗，治疗原则是：消除病原和增强机体抵抗力。全身应用广谱抗生素及磺胺类药，大剂量连续使用，直至体温降至正常后2-3日。大量补充水分和营养成分，防止酸中毒，增强心脏活动。静注糖盐水、5%碳酸氢钠、维生素c，肌注复合维生素B、安钠咖等。肌肉注射催产素促进子宫内分泌物及分解产物排出。遗留腐败胎衣必须清理干净。体表局限性脓灶可以外科处理，但只能缓解症状。本病宜精心护理，喂以营养丰富易消化的饲料，充分饮水，加厚垫草，及时清理污草，定时翻转身体等。
曹光贤九牛牧业助理兽医师 经过前辈们的尝试探索和实贱，对此病有着多种行之有效的的治疗方法，引起我对此病的思考。我根据自己多年的临床经验分析加以剖解与大家分享，如有不足之处望大家谅解。瘫痪又叫卧地不起综合症，一般兽医认为是缺钙引起的，其实不然，怎样才能行之而有效地把卧地不起的牛治愈。一名专业的兽医在没有化验室的情况下，把奶牛瘫痪病的治愈率达到98%，那是何等的了得。 奶牛产后瘫痪是奶牛分娩前后一种严重的代谢病又称乳热症，主要特征为全身肌肉无力，知觉丧失及四肢瘫痪，主要发生于3～6胎的高产奶牛和肥胖牛，有的养殖场发病率高达20～25%，如不及时治疗有50～60%的病牛可能在1～2天内死亡。 一、发病原因 1.低血钙; 2.低钾血症; 3.低磷血症; 4.低鎂血症; 5.瘤胃酸中毒; 6.产后截瘫; 7.热射病;、 8.乳房炎继发症; 9.外伤性得瘫痪; 10.风湿性瘫痪。 二、临床症状 典型症状发生在产后3天内，发病突然，奶牛迅速瘫痪，卧地头颈失去平衡，弯向胸侧，拉直后松开仍回复原状，意识抑制，瞳孔散大，对光和疼痛无反应昏睡，体表末稍发凉，体温低于35℃～36℃，有的病牛发生喉头麻痹等现象，病牛死前大多处于昏迷状态。非典型症状多在分娩前后的很久才发生，症状不明显，头颈姿势不自然成S状弯曲，体温正常
或偏低，食欲废绝，精神极度沉郁但不嗜睡，各种反射减弱但不完全消失，有时也能勉强站立，但不稳且行动困难，步态摇摆。 三、诊断 奶牛临产前后处于特殊的生理状态，致使代谢及不稳定因而出现卧地不起瘫痪症状。 1.低血钙症多发生在产后三天内，典心的卧下时头与躯体呈S状弯曲，补钙有效，可以迅速提高血钙水平消除脑贫血和缺氧状态，且治疗越早越好。 处方：10%糖酸钙1000ml，地塞米松20mg或可的松25mg，50%葡萄糖500～1000ml，VB1 50ml静注。 2.低钾血症体温39.6 ℃，心率90次/min，呼吸30次/min，精神沉郁食欲减退卧地不起针刺激敏感，强迫患牛站时前肢能馈起但后肢无力难以支掌挣扎后被迫横卧与地上，可视黏膜潮红，鼻镜湿润反刍，嗳气减少，瘤胃蠕动无力排稀软粪便，瞳孔后驱及四肢反射无异常。 处方：0.9%氯化钠2000ml，10%氯化钾16g，25%葡萄糖1000ml，5%葡萄糖1000ml，加能量合剂25%，MgSO2 100ml，VB150ml静注。 3.低磷血症体温37.4℃，心率90次/min，呼吸30次/min，躺卧不起，常回视后驱，步态紧张，四肢僵直吼叫。钙治疗无效。可视黏膜正常。精神淡漠。反应迟钝。 一般可分为(1)骨软型该病多见，食欲不振或废绝，有异食现象，弓背肩关节外展，关节肿胀，四肢强直颤抖，跛行喜卧，站立或行走时呻吟，严重时卧地不起，易骨折。(2)血红蛋白尿型体温正常或稍高，可视黏膜苍白。食欲不振呼吸快。脉搏增速。排尿多呈红色以后变成茶色。最后变成酱油色。有全身症状死亡率高。(3)混合型病牛兼有上速俩种类型，上述症状可同时发生。 处方：5%葡萄糖1500ml,20%磷酸二氢钠500ml，10%氯化钾30ml，0.5氢化可的松40ml缓慢滴注。 4.低鎂血症除瘫痪症状外，主要表现四肢抽蓄肌肉震颤，角弓反张，呈强直性或发作性痉挛，反射亢进，心动过速。血清鎂含量下降1.2mg以下，25%葡萄糖1000ml，地米20ml，25%硫酸镁100ml，10%葡萄糖1000ml静注。 5.瘤胃酸中毒除有瘫痪症状外还有腹泻。脱水不反刍CO2结合力降低，嗳气及胃内容物呈酸臭味，pH降低到4.0，应用小苏打和洗胃等对症治疗。 处方：5%小苏打5000～1500ml，复方盐水500～2000ml，安纳加20ml，VC 50ml。 6.产后截瘫多有产道狭窄，胎儿过大，助产牵引过猛或产后摔倒病史患牛全身状态好，只是后驱站不起来。 四、治疗原则
奶牛繁殖程序 北京龙德农业有限公司钟海 奶牛的繁殖一直是牛场管理的一项主要工作，繁殖率的高低直接影响到牛场的经济效益。而目前很多的牧场还只是停留在发情配种，自然观察，发现多少配多少的阶段。为此，奶牛的繁殖应该是有一套相应的程序进行管理，以提高奶牛的正常发情，配种受孕。 一、助产标准 1、提倡自然分娩，奶牛出现分娩征兆后10分钟未发现犊牛露蹄和嘴时，进行胎位检查。 2、羊膜囊破裂后，奶牛无怒责时，实施助产。 二、产后管理 1、胎儿产出后，立刻进行母牛产道检查，注意出血及撕裂受伤。 2、奶牛产后立刻饲喂麸皮红糖水。 3、肌肉注射缩宫素100单位，V ADE10ml。 4、要求在产后半小时内立即驱赶奶牛站立。 三、产后护理 1、产后奶牛的体温监测：夏季：39.5℃、冬季：39.2℃（特别注意炎热季节体温变化）。 2、产后12小时不见胎衣称为胎衣不下，不主张手术剥离，可配合药物治疗实行保守疗法。
3、胎衣不下牛注意体温变化，出现感染可进行输液，配合子宫投药。 四、产后牛繁殖护理 1、观察恶露排出情况，注意恶露滞留、恶露颜色异常。 2、产后11~13天肌肉注射6~10mg雌二醇。 3、产后15~21天检查子宫复旧情况，通过检查可刺激子宫恶露排出。 4、产后18~21天肌肉注律胎素半支，促进内容物的排出。 5、产后28~30天第二次直肠检查，发现子宫炎症牛进行投药治疗。 6、产后45天子宫必须净化，等待自然发情。 7、产后60天出现不发情牛立刻进行处理。（因随着产奶量越来越高，子宫恢复期延迟。另子宫炎牛处理不及时，容易形成子宫蓄脓、子宫黏连、输卵管炎及卵巢炎）。 五、产后牛理想配种时间 1、头胎日产30Kg，70天以上配种。 2、头胎日产20Kg，60天以上配种。 3、经产日产小于20Kg，45天以上配种。 4、经产日产小于25Kg，60天以上配种。 5、经产日产大于35Kg，70天以上配种。 六、发情观察 1、夏季早班观察时间应在挤奶前进行。
奶牛生产性能测定科普读物 第一章奶牛生产性能简介 （一）什么是奶牛生产性能测定 奶牛生产性能测定,是对奶牛泌乳性能及乳成分的测定,通常用DHI（Dairy Herd Improvement）来简称,其含义是奶牛群体改良,具有一套完整的奶牛生产性能记录体系。 首先需要收集奶牛系谱、胎次、产犊日期、干奶日期、淘汰日期等牛群饲养管理基础数据，其次是每月采集一次泌乳牛的奶样，通过测定中心的检测，获得牛奶的乳成分、体细胞数等数据，然后将这些数据统一整理分析，形成生产性能测定报告。测定报告反映了牛群配种繁殖、生产性能、饲养管理、乳房保健及疾病防治等方面的准确信息。牛场管理人员利用生产性能测定报告，能够科学有效的对牛群加强管理，充分发挥牛群的生产潜力，进而提高经济效益。同时，它也是奶牛育种工作的基础，是评估公牛遗传素质最重要的数据来源，是提高奶牛群管理水平和生奶质量水平的有效工具，并为乳业科学研究提供准确的数据。 （二）国内外奶牛生产性能测定的发展与现状 在国外，奶牛生产性能测定自1907年诞生以来，经过100年的发展，已经逐渐演变为综合的牛场管理方案，旨在向奶农提供全面的牛场管理信息。1953年，美国、加拿大两国正式启动了“牛群遗传改良计划”，即奶牛生产性能测定。目前加拿大已有70%的牛群参加生产性能测定，美国有45%的牛群参加生产性能测定，奶牛单产水平最高的以色列参加生产性能测定的牛群高达90%。几十年的发展证实，美国、法国、荷兰等奶业发达国家通过应用奶牛生产性能测定这一先进体系来为奶农提供指导服务，产生了巨大的经济效益，奶牛的单产水平均已达到9000—10000千克。 在我国，奶牛生产性能测定起步较晚，1992年在“中日奶业技术合作项目”的扶持下，天津启动了奶牛生产性能测定工作；1995年随着中国--加拿大奶牛综合育种项目的实施，
谈-奶牛产后护理的重要性 汶上牧场-李树超从2013年6月-2018年4月，转眼间，我已在现代牧业兽医团队工作将近5年，兽医是一个牧场奶牛健康的“护卫”，技术支持中心郭总说过：“在新时代规模化的牧场的前提下，每名兽医，必须遵循以“食品安全，防疫安全”为核心，以“预防为主，防重于治”为理念，才能成为1名合格的兽医。”简简单单16个字，突出牧场兽医职责与奶牛健康的重要性。 众所周知，一头成母牛在分娩后有三个高风险的评估阶段：产后能量负平衡，低血钙和子宫炎。所以，初产牛的产后护理非常重要，除了合理的饲养管理外，在疾病预防方面，我们必须以“奶牛健康，先发制人”为原则，按照产后护理流程做到“早发现，早治疗”，才能在产后50-60d达到理想的泌乳高峰，提高60d发情揭发率和产后90d发情鉴定率，缩短产犊间隔，达到健康，高产，稳产的牛群结构。 所有初产产后牛与经产产后牛需要分栏饲养，且牛群密
度不能超过80%，产后护理牛只都需要遵循以下三个各方面“产后镇痛，预防低血钙，产后检查” 一．产后镇痛 对于所有助产牛（包括1级助产，2级助产，难产），在产后第一时间进行镇痛处理。肌内注射非甾体抗炎药,对于有产道拉伤和产道损伤的牛只根据产道撕裂形状，长度，深度决定是否缝合，并进行局部相应处理治疗。 二．预防低血钙 对于经产牛进行投服博威钙，产后2h内进行投服1枚。（≧3胎）经产牛在产后12-18h投服第2枚。 三．产后检查 总结为：1测，2看，3观察，4全面； 1.监测体温 对于产后牛进行每天体温监测。≧39.5℃判为发热，需要进行治疗。（其中，2/3的奶牛发热是由子宫炎引起，1/5的发热是由乳房炎引起，需要按照相应的流程进行治疗；）39.1-39.4℃需要关注，重点观察奶牛采食，反刍和躺卧行为；38.4-39℃属于正常体温；<38.4℃，需要关注，重点观察奶牛精神，采食，反刍，步态运行（是否发生败血症，蹄病等）。 2.观看乳房充盈度 挤奶过程中，1名兽医站于前药浴挤奶工与擦毛巾挤奶
东北农业大学毕业说明书奶牛产后瘫痪的防治
目录 摘要 (1) 1 病的发生 (1) 2 病因 (1) 3 症状 (3) 4 预防 (3) 4.1 加强干奶期特别是围产期奶牛的饲养管理 (3) 4.2 干奶期饲喂优质粗饲料 (3) 4.3 提供良好的饲养环境 (3) 4.4 补充钙磷 (4) 4.5 注意事项 (4) 5治疗 (4) 5.1钙剂疗法 (4) 5.2乳房送风 (4) 5.3辅助治疗 (5) 5.4对症治疗 (5) 6 结束语 (5)
奶牛产后瘫痪的防治 摘要：产后瘫痪又称生产瘫痪，是奶牛分娩后突然发生的一种以体温下降、四肢麻痹、卧地不起、知觉丧失并伴有咽、舌及肠道麻痹等为特征症状的代疾病。该病广泛存在于世界各地，是奶牛饲养中的一种常见病。本文从营养缺乏、产道损伤、心包创伤、产后感染、产后出血等方面详细论述了产后瘫痪综合征的致病原因，并阐述了其临床症状，提出了详实可行的防治措施，从而提高了诊断的准确性和防治效果。 关键词: 奶牛产后瘫痪预防治疗代疾病发病率 产后瘫痪又称生产瘫痪，是奶牛分娩后突然发生的一种以体温下降、四肢麻痹、卧地不起、知觉丧失并伴有咽、舌及肠道麻痹等为特征症状的代疾病。该病广泛存在于世界各地，是奶牛饲养中的一种常见病。主要发生于饲养良好的高产奶牛，而且出现于产奶量最高时。虽然为散在形式发病，然而个别牧场的发病率可高达25％～30％。治愈的奶牛下次分娩可能再次发病。近年来，随着奶牛业的迅速发展，这种疾病也日趋增多，对奶牛业的发展有很大的影响。 奶牛产后瘫痪综合征是临床上的常见病、多发病，形成的原因多种多样，病因极其复杂，从而给临床的有效防治带来了一定的难度，根据本人的临床实践和体会，下面介绍本病的综合病因及其防治。 1 病的发生 大多数在产后3天发病，5～10岁、产犊3～6次的母牛发病最多，愈是高产牛，发病愈多。发病与犊牛性别、体重大小、死胎和双胎无关。上一胎泌乳期缺钙症是下胎泌乳期乳热增多的因素；发生过胎衣不下、子宫炎、酮病等症，有使乳热发生增高的倾向。干奶期营养状况与本病的发生有关： 1.1干奶期精料喂量过多，特别是日粮中的蛋白质水平过高，则对此病更为易感； 1.2产前饲喂高钙日粮、饲喂高阳离子Na+，K+和低阴离子Cl—、S—日粮，都易促使发病。临床发现，发生过产后轻瘫的牛，下胎产犊后，有重复发病的趋势。因此认为，本病是一个能复发和遗传的疾病。发生过乳热的牛比未发生过乳热的牛易感性高2～5倍。产后瘫痪是危胁奶牛生产较为严重的疾病之一。如失治，容易造成奶农及奶牛饲养企业极大的经济损失。为了弄清本病的发生原因，建立正确的诊断和治疗方案，笔者从1991年起收集了大量相关资料，并从临床上进行验证。发现引起奶牛产后瘫痪的原因是多方面的，因此其临床表现和治疗方法也不相同。 2 病因 2.1大量钙质随初乳进入乳房，奶牛血钙浓度急剧降低是造成本病的主要原因。也是引起本病典型症状的基础。干奶期，母牛对钙的需要处于最低限度。胎儿的发育、尿液和源性粪
奶牛保健程序1
奶牛保健方案 一、乳房炎的预防保健 1、乳房炎的发生 乳房炎是对奶牛生产危害最大的疾病,平均发病率高达40%-65%,其中临床型乳房炎的平均发病率为2%-3%,隐性乳房炎的平均发病率为38%-62%。 乳房炎的发生与饲养环境、饲养管理、挤奶设备的正确使用与保养，挤奶程序等因素密切相关，其中，不正确的挤奶程序是引起感染的主要原因。 2、正确的挤奶和保健程序 （1）温和地待牛。牛在挤奶过程中，由于乳头部位的神经末梢受到刺激，促使脑垂体释放催产素，使乳汁排出。如果使牛受到惊吓，牛则会释放肾上腺素，从而抑制催产素释放，影响产奶量。 （2）清洗乳头。清洗乳头目的一是刺激乳头，二是为得到干净的牛奶。清洗乳头有3个过程：淋洗、擦干、按摩。淋洗时注意不要洗的面积太大，因为面积太大会使乳房上部的脏物随水流下，集中到乳头，使乳头感染的机会增加。淋洗后用干净毛巾擦干，注意一牛一巾，用后清洗消毒。然后按摩乳房，促使乳汁释放。 （3）废弃最初的1～2把奶。这样能使挤奶工人及早发现异常牛奶和临床型乳房炎，从乳导管中废弃含有高细菌数的牛奶，提供一个强烈的放乳刺激。
（4）乳头药浴。专家建议，挤奶前用“至高点”400倍稀释消毒药液浸泡乳头后，然后停留几分钟，再用纸巾或毛巾擦干。。在环境卫生较差或因环境问题引起乳房炎的牛场实施这一程序非常有必要。 （5）挤奶。如果是机器挤奶，应注意正确使用挤奶器，并观察挤奶器是否正常工作。 （6）挤奶后药浴乳头。张开的乳头乳极易受环境性病原菌的侵袭，挤奶结束15分钟后，乳头的环状括约肌才能恢复收缩功能，关闭乳头乳。每次挤奶后1 分钟内要及时药浴，持续5秒钟，消毒液附着在乳头上形成一层保护膜，可以大大降低乳房炎的发病率。3、乳房炎的治疗程序 （1）纯中药疗法：乳炎消或乳炎奇效，10ml×5支，肌注或静注，2次/日；乳肿消口服，1-2袋/日；消炎膏外敷；以上3天一个疗程。（2）中西结合疗法：炎康或宫乳奇效10ml×5支，静注，2次/日；乳炎消或乳炎奇效10ml×5支肌注，乳肿消口服，1-2袋/日；消炎膏外敷；以上3天一个疗程。 二、产后瘫痪的预防保健 1、奶牛产后瘫痪又称乳热症，是奶牛，特别是高产奶牛或分娩胎次较多的奶牛在产后发生的一种急性低血钙症。通常在产后12～72h 发生。 2、病因
奶牛产后酸中毒的诊治 临床症状 患病奶牛都发生于产后3天内，而且都是高产或有难产史的奶牛。本病发生迅速，病初奶牛精神沉郁，食欲减退，肌肉震颤，瘤胃蠕动音减弱，步态蹒跚，站立不稳，喜卧。后期食欲废绝，反刍停止，流涎，瘤胃蠕动音消失，病牛趴卧不起，排水样稀便，有酸臭味，有的有时有血丝。产奶量下降，眼球凹陷，皮温不整。体温正常或稍低，心跳加快，每分钟可达100次，呼吸加快。如治疗不及时，会导致死亡。 病理解剖学变化 对1例重症死亡牛进行解剖，主要是消化道充血、出血、水肿、黏膜坏死和实质器官的水肿、退行性变化。 瘤胃内容物呈酸臭味，混有血丝；瘤胃黏膜脱落、坏死，呈暗红色，有出血；真胃黏膜脱落、出血；小肠内容物暗红褐色，肠黏膜出血、脱落、坏死，肠壁水肿；肺脏呈现瘀血、水肿；心脏右心室扩张、柔软，有出血；肝脏表现为脂肪变性、瘀血，有坏死灶；肾脏色淡、肿胀，质地柔软；淋巴结水肿；脾脏萎缩；外周血管血液黏稠，呈暗紫色。 治疗 （1）禁喂精料和限饮，防止继续酸中毒。用碱性溶液洗胃，胃管经口腔插入瘤胃内，排出液状内容物，用石灰水（石灰与水比例为1∶6，用上清液）8000毫升左右，反复冲洗，直至瘤胃呈碱性为止。 （2）全身疗法，缓解酸中毒。以5%碳酸氢钠溶液1000毫升～1500毫升静注，当pH值达6.7时，应停注，同时用5%葡萄糖生理盐水1000毫升、5%维生素B120毫升、5％维生素C40毫升静注。（3）对症
疗法，防止继发感染。可用10%安钠咖10毫升肌注，还可用庆大霉素等治疗。 （4）经过2天～3天的治疗，病牛能站立或有食欲时，可先给予少量优质干草以促进胃肠蠕动，或以下列中药1剂～2剂灌服。当归50克，元芪50克，党参30克，榔片40克，陈皮30克，川朴30克，草果30克，五味30克，豆蔻30克，麦芽粉100克，酵母片60片。共为细末，开水冲，待温服。一般3天～4天可治愈。
产后监护管理程序 体温升高 1. 正常产犊 (1)查找是什么原因引起温度升高的。 (2)检查乳房是否有乳房炎(和正常牛只分开挤奶、采样做细菌培养，尾根2ml垂体后叶素注射，用40～50度温水擦乳房，用广谱抗生素、美达佳、钙、碳酸氢钠、糖盐水治疗，并根据实验室结果选择对细菌敏感的抗生素治疗)。 (3)如果查不到原因(无名热)：采用子宫收缩药、美达佳、广谱抗生素(辉瑞速解灵、易速达)、补液治疗。体温正常后还要巩固1～2天。 2. 非正常产犊 (1)胎衣不下：a.产犊后12～18h，美达佳、广谱抗生素(辉瑞速解灵、易速达)、抗炎药、退热的，气温32度以上的，第二天注射美达佳、广谱抗生素(辉瑞速解灵、易速达)、抗炎药、退热的、补液、碳酸氢钠治疗。 (2)难产、胎儿过大、双胞胎、助产过度：新产牛疼痛感表现：踢腹，收腹，呻吟，烦躁不安，眼睛无神，拱背。 (3)观察有无恶露排出(没有恶露用PG（氯前列烯醇）5ml，雌二醇2mg注射;检查子宫有无破裂。使用广谱抗生素(辉瑞速解灵、易速达)、补液、碳酸氢钠、美达佳治疗)。 体温正常 1. 正常产犊：连续10天体温监控，如果体温升高的按体温升高方案处理。 2. 非正常产犊：第一天用子宫收缩药注射，第2～10天连续体温监控，观察牛只精神，食欲变化。 体温正常食欲废绝(检查代谢病) 1. 正常产犊：a.检查酮体，补充葡萄糖，糖皮质激素。b.检查消化系统，胃肠蠕动音弱(健胃药灌服，促反刍液、碳酸氢钠、糖钙治疗)，皱胃变位手术治疗，补充能量。 2. 非正常产犊：(难产、胎衣不下、产道拉伤，双胞胎)头孢噻呋(海正)25ml，连续3天，有疼痛现象非甾体药物肌注。 产后瘫痪 采血样检测Ca、P水平，根据情况补充钙，效果不明显的，8h后重复一次，硝酸士的宁25ml百会穴注射，或者看哪个牛肢体无力就在那个牛肢体皮下注射。 产后保健方法 1. 产后汤灌敷(30kg)：丙二醇300ml，红糖500g，酵母20g，益母草膏500g，食盐30g。温度20～30度。这样能迅速补充能量、填充腹腔的空虚减少四胃疾病的发生。 2. 补钙(博威钙)的投服：产后投服一枚，体质差牛只在12小时后重复投1次 3. 对产道损伤、难产、助产、胎衣不下，双胞胎牛只每天1次头孢噻呋(海正)25ml，连续3天 4. 有疼痛的牛只注射非甾体药物(美达佳)，3天1次。
奶牛产后常见疾病的防治 产后奶牛在产后7～10天阶段，每天要认真检查产后奶牛的体温、精神、采食、反刍、肢蹄、恶露颜色、乳房充盈度、瘤胃充盈度、子宫排泄物和粪便形态等情况并做好分析记录。要注意产后奶牛分娩后胎衣脱落排出的时间和子宫排出物的形态、颜色和气味等情况。正常的情况下产后奶牛一般在12～24小时以内就能自行排出胎衣。超过时间就应视为胎衣滞留，应及时采取相应的诊治措施，防止产后奶牛胎衣在体内长时间滞留。对于双胎、早产、难产、死胎、瘦弱、庝痛等的产后奶牛及时进行全身检查，及早诊疗，促进康复。体况评分:要求产后奶牛体况分值3.5～3.75范围以内。对于体况偏差的产后奶牛要加强饲养管理，促使体况达到标准要求。 1、每周进行一次产后奶牛酮病检测：对检测结果为3+的产后奶牛，须注射B族类维生素，灌服丙二醇等药物予以早期预防治疗； 2、预防低血钙、产后瘫痪、酮病等产后常见疾病：每1～3天抽血检测一次血钙水平和酮体、BHBA水平。根据实验室检测数据指标，采取相应预防措施。也可灌服以下配合预防药物：丙酸钙450～500g、氯化钾100g、硫酸镁220g、酵母200～300g、阿斯匹林粉45～50g、25度左右温水30～50L。其中钙制剂可以视情多灌服2～3次； 3、对产道拉伤和庝痛严重的产后奶牛：每2天用消毒液、凡士林、消炎粉等药物处理创面；肌肉注射镇痛消炎药缓解疼痛，消炎消肿；
4、预防产后奶牛胎衣滞留：可注射缩宫素促进胎衣排出。即在奶牛产后1、4、7小时分别注射40IU催产素，第二天如胎衣仍没有排出，可再注射适量前列腺素促进胎衣排出。如果注射药物无效，就需要采用子宫冲洗注药的方法促使胎衣排出。具体方法如下：先用消毒药液将产后奶牛的外阴处清洗干净。用手臂将将已消毒过的透明塑料软管送入阴道，再通过子宫颈到达子宫低垂部后引导出子宫恶露。然后经软管注入5%～10%糖盐水500～1000ml溶液冲洗子宫，导净子宫内的存液后，再注入土霉素5g、利凡诺0.5g、生理盐水 500ml。每隔一天一次，直至滞留胎衣排出； 5、防治子宫炎：对感染子宫炎和子宫内膜炎的产后奶牛及产后30天子宫还没有正常复原的产后奶牛，可采取抗菌素进行子宫冲洗的治疗措施。对于严重感染的牛可以每隔3天再连续冲洗3次子宫的治疗办法。常用于治疗子宫内膜炎的药物有抗菌消炎、激素、防腐类等药物。可用40℃左右的0.1%～0.3%高锰酸钾200～300ml冲洗子宫，同时可用手经直肠按摩提压子宫，促使药液能将子宫冲排干净。尔后再取青霉素160万U和链霉素100万U溶于无菌水100ml,注入子宫消炎。或取土霉素粉2～3g溶于100ml生理盐水中后注入子宫消炎。对病情较重、子宫肥厚、不断排出脓性分泌物，已转化成慢性子宫内膜炎的产后奶牛，可肌注乙烯雌酚20mg或脑垂体后叶素100U促使子宫收缩，进行配合治疗。产后奶牛冲洗子宫一般每2天一次，一个疗程视情冲洗子宫3～5次。当产后奶牛体温≥39.5℃，采食、反刍减
综合治疗奶牛产前产后瘫痪 奶牛产后瘫痪症，属于家畜产科疾病的范畴，目前在我区奶牛养殖场时有发生，也是兽医临床上较难治疗的一种常见病，若不及时治疗可造成淘汰，给养殖户带来很大经济损失。笔者自2000年以来在兽医临床上采取综合性的治疗措施，缩短病程，提高疗效，节省开支，安全可靠，无副作用。治疗50例产前产后瘫痪病例均取得了满意的效果。据临床资料记载，产后瘫痪多于产前瘫痪，特别是高产和体质较差的奶牛多发，多在产后1～6天发病，最急者产后1～3小时即可卧地不起而发病；产前瘫痪多在产前7～26天左右发病较高，有特殊病例在怀孕4～5个月而发病。究其原因是由于母畜机体内环境发生急性代谢紊乱及饲养管理不当而引发，在妊娠期间营养比例失调，长期缺乏微量元素及矿物质钙磷，或长期缺乏运动及光照造成畜体血钙量过低，营养不良，生化无源，久而久之，气血双亏，血循滞缓，血不养筋而呈现肌酸肢麻，导致卧地不起而瘫痪。 发病年龄一般在3～8岁的高产奶牛，体质不良、年龄越大的奶牛发病率越高，一年四季均可发病，但晚冬早春两季多见。该病发病较急，多呈慢性经过，对产后的奶牛要加强饲养管理，注意观察，及时治疗，可获得理想的效果。 1 发病原因 多因对怀孕的母奶牛饲养管理不善，饲草料单一，营养不足，生化无源，造成气血双亏。大量营养物质得不供给，机体素虚，特别是妊娠期的母牛更急需大量营养物质的供应，而营养匮乏，饲料中钙磷严重缺乏，致使血液中的血钙不足，进一步造成体内管状骨的骨密度疏松；或者因甲状腺机能紊乱，引起钙磷的吸收障碍；或者在怀孕期后及产后泌乳量过大的奶牛大量的血钙被消耗，导致体内应激性降低而呈现瘫痪的症状。再者是由于母牛在妊娠期特别是后期胎儿快速生长，需要大量的营养物质，尤其是钙磷的需要，长期缺乏运动和光照，造成机体微量元素矿物质及维生素的缺乏也是引起奶牛瘫痪的主要原因之一。 2 临床症状 奶牛的瘫痪症轻者表现精神不振，食欲、反刍、嗳气减少，泌乳量下降，不愿行走，行走时四肢不灵，后肢向外展，摇摆，喜卧地不愿站立，强行站立似昏睡，食欲、反刍、嗳气减少或停止。前期行走步态不稳，后躯摇摆，转弯运动时易摔倒。严重者，卧地瘫痪不起。肌肉较丰满的部位颤动，多数四肢积于腹下。严重者后肢张开，呈麻痹状态，针刺不敏感，反射性极差，大小便失禁，头颈变向一侧，大多患畜似犬卧姿势，低头，眼闭耳耷。体温多数在37℃左右，心跳缓慢，呼吸深缓，伴有痰鸣音，鼻镜湿润，汗不成珠，有时无汗，有时磨牙和发出吭吭声。
奶牛产前产后的护理方案 北京邦士富生物科技有限公司技术部赖利兄我们发现，如果不注重奶牛产前产后饲养管理的实施，或者实施了错误的护理方法，奶牛的产科和代谢类疾病就会接踵而至，例如，乳房炎，乳房恶性水肿，乳热症（产后瘫痪），酮血病，酸中毒，瘤胃积食，胎衣不下，真胃移位，真胃积食，真胃炎，奶牛产后综合症等，轻则花费巨大的治疗费用，造成奶牛产奶量下降，影响经济效益，重则治疗不愈，不得不淘汰奶牛。为此，我们从饲养管理和预防措施上，提出一些产前产后的护理方法来避免和减少上述问题的发生，以保证奶牛产前产后正常的生理和代谢过程。 产犊前的护理方法 1、在预产期前21天，要增加精补料的营养水平，减少精补料的喂量，每天不超过4kg，多喂优质牧草。可预防真胃移位，真胃积食，真胃炎等 2、不能喂块根、酒糟、豆腐渣等多汁类饲料。 3、产前不要再饲喂玉米青贮饲料。 4、不能饲喂苜蓿干草。 5、产犊前21天，加强运动，每天至少运动6小时。可预防和减少胎衣不下。 6、产犊前21天，奶牛的日粮中，盐、钙、磷的水平不能太高，否则会引起奶牛的乳热症（产后瘫痪）。
7、产前21天，日粮中增加维生素和微量元素的浓度，另外添加反刍动物酵母培养物。 8、要把产前21天的奶牛与其它干奶牛隔开，有条件的牧场要提前把临产奶牛放进单独的产房，注意观察奶牛的情况，一旦发现异常，及时处理。 9、产前5天到产犊，最好停喂或少喂精补料。 产犊后的护理方法 1、立即给分娩后的奶牛披上薄棉被或其他覆盖物，预防感冒。 2、产房或棚圈应封闭，防止冷风直接吹在奶牛身上。 3、清理地面的胎衣和污物，然后进行环境喷雾消毒。 4、立即用聚维酮碘给奶牛的外阴清洗，消毒。 5、产后给奶牛补液，消炎，止血。 方法：（1）5%葡萄糖盐水1500ml+头孢噻呋钠和甲磺酸培氟沙星混合，一次静注。 （2）（10ml）安络血5支一次肌注。 6、产后4-5天内，每天给奶牛饮一次营养粥。 配方是：麸皮+红塘 +扶正解毒散250g，用10-15kg开水冲开，候温饮用。连用5日。 7、产后3天内，不要饲喂精补料，3天后，根据奶牛不断上升的产奶量，逐步添加精补料，但每天不超过。 8、产后给奶牛多喂一些优质粗饲料。例如，羊草，苜蓿干草，优质青贮。
闫克山韩己武邢映琨北京中博农畜牧科技有限公司 近期，有幸随着“国家奶牛产业技术体系”金钥匙奶业培训会议到几个省市的一些规模牧场考察，以及和当地一些养殖户进行奶牛饲养管理交流，考察交流过程中关于奶牛接助产后产道损伤和护理的问题很多，现就奶牛在接助产过程中遇到的一些问题做简单的阐述。 在实际生产过程中，奶牛产犊过程中发生难产的因素很多，母牛配种过早，个体小导致产道狭窄，产道损伤；奶牛过度肥胖，造成盆腔蓄积脂肪过厚，引起产道狭窄；瘦弱无力，不能产出胎儿，胎儿过大、畸形、死胎、胎位异常、胎势不正也会发生难产。对干奶期母牛要加强饲养管理，多喂一些优质的牧草，严禁喂给霉败和不易消化的饲料；舍饲牛栏不得过于拥挤，经常保持清洁，干燥，并给予适当运动和阳光照射。此外，青年母牛初配体重不易太小。发生难产时应根据具体情况，适时进行助产，方法简单介绍如下： 一、助产前检查 1、首先要了解母牛分娩开始的时间，是初产或经产、胎膜是否破裂，有无羊水流出，腹围及母牛大小，检查母牛震缩和努责是否有力，初产青年母牛常因产道狭窄而难产；经产母畜的难产多由于胎儿的位置、方向、姿势不正。 2、检查产道是否有粘膜水肿、表面是否干燥和润泽以及有无出血损伤，并注意产道损伤的程度及有无污染和感染。 3、通过产道检查胎儿时，应注胎位、胎势、胎向是否正常以及胎儿是否生存和死亡。 4、检查母牛的全身情况，如精神状态、脉搏、呼吸等，如出现过弱或亢进，心率不齐，要进行输液或强心等治疗措施。 二、助产前准备 1、将能站立的母牛置于合适的体位站立保定，如不能站立的可将母牛侧卧于有柔软垫料的地面保定助产。 2、将助产者的手臂和胎儿露出母体的部分及母牛的会阴、尾根努处用温水洗净，并将牛尾用细绳拴于体侧，再用0.2％新洁尔灭溶液消毒会阴。 3、所需接助产器械应要做好仔细消毒；并将2-4条助产棉绳用消毒液浸泡柔软以作牵引胎儿用。 三、助产注意事项 1、首先要把胎儿送回产道或子宫腔内、再矫正胎儿的方向、位置、姿势。 2、强行牵拉胎儿时，操作者配合母牛努责的频率指导其他助手牵拉胎儿的力量、方向和时间，以免损伤产道。注意参与的助手不宜过多，以免造成过度强行牵拉，致使产道撕裂或胎儿损伤。 3、为了滑润产道和保护粘膜，对难产母牛的产道可注入消毒过的人造石蜡油和药用软皂等润滑剂。
奶牛产后科学保健措施 奶牛产后7d内，食欲减退，体质弱，抵抗力差，营养 严重缺乏，这往往是各种疾病侵入的最佳时机，常见的疾病有产后热、不食、产后瘫痪、子宫内膜炎、酮病等。所以做好奶牛产后7d的保健，特别重要，不仅可以奶牛的体质尽 早的恢复，抵抗力增加，减少和预防产后各种疾病发生，还可使产奶高峰期更快的到来，奶牛以后的正常发情时间，保证奶牛后期正常的生产性能。 1日粮与饲喂 1.1精料 若饲养过于丰富，特别是精料给量过多，会引起消化功能紊乱，加重乳房水肿或发炎。对于体况很好的奶牛来说，第一天少给或不给精料，第二天逐步增加，而3d内的精料 量应控制在1kg左右，少喂勤添。第四天在此基础上开始增加；对于体况差的奶牛，前3d不给精料，第四天开始少量 饲喂。第七天以后产后牛群按正常的日粮配方饲喂，在此过程中一定要观察奶牛的采食状况和消化功能，确定其增加量。 1.2粗饲料 产后3d内，主要以质量较好、易消化的优质牧草为主、奶牛自然采食，每天的饲喂量不低于3kg，不喂或少喂多汁
类饲料，青贮饲料等，根据个体差异、食欲是否正常而决定，4d后增加青贮的饲喂量，保证瘤胃的正常发酵，精粗饲料比例要合理，防止胃酸过多而引起酸中毒。并且饲料中的钙的含量要达到0.6％以上。 2管理 2.1饮水 奶牛产后水分大量流失，身体虚弱，要立即饮温热，充足的麸皮—红糖水，比例为：温水（37～38℃）10kg，麸皮1kg，红糖500g，有条件的加入速补钙1000mL。1周内坚持饮温水，1周后，降至常温。如有1头奶牛产犊后，身体虚弱，张口喘气，浑身出汗，及时服用麦麸—红糖水，还加入了两瓶速补钙，大约15min后，奶牛的外部表现基本恢复正常，之后的1周内，每天坚持服用温水冲服的麦麸—红糖水，奶牛的食欲、体况逐渐恢复，效果显著。 2.2运动 产后奶牛要加强户外运动，对胎衣排出，子宫、体质恢复起到非常好的作用，并且阳光充足时可以促进钙的吸收，防止瘫痪。如果是冬季，每天中午阳光充足时，可以将产后奶牛赶到运动场里，加强运动；在春夏秋季，让产后母牛在运动场里自由活动、自由采食，不要人为的去干扰，确保奶牛的运动量。
奶牛产后瘫痪的发病原因及治疗措施 四川奶业2009年2期 奶牛产后瘫痪的发病原因及治疗措施 近年来,奶牛养殖业发展迅速,己成为 广大农户致富的有效途径.但奶牛产后瘫痪, 尤其是高产奶牛产后瘫痪发病率的明显增 高,严重影响着奶牛业的发展.通过十几年 的临床实践,就谈病的发病原因及治疗措施 介绍加下. 1发病原因 奶牛产后瘫痪,是奶牛产后1～3d,以昏 迷和癣痪为特征的急性低血钙症.多发生于 5-9岁高产奶牛.病牛大多是由于甲状旁腺 机能衰竭,引起血钙调节机能失调.在高钙 饲养条件下,甲状旁腺机能降低,分娩后骤 然泌乳,随着大量钙的流失使血钙低下,而 不能引起甲状旁腺素的充分分泌,使骨钙动 员迟缓,肠道对钙的吸收减少,从而导致低 血钙症,其总钙和游离钙水平的降低可延迟 到分娩后数天.当血钙降低时,向镁相应增 高,神经肌肉的应激性增高,故有时见到抽 搐症状. 2临床症状 奶牛产后瘫痪的症状分3个阶段. (1)前驱阶段:表现为兴奋不安,紧张 乱动,对刺激敏感,采食,排尿及排粪停止, 头和四肢震颤.
2.4抓好繁殖配种工作掌握青年母牛初 次配种的适当时间:奶牛一般在1820个月龄,体重达到350kg(为成年母牛体重的65% ～ 70%)时,开始配种.保持适当的产犊间 隔,实践证明,产犊间隔以351～395天的奶牛平均产奶量为最高.调整分娩期:把高产 的母牛安排在冬,春季产犊,能有效地提高 产奶量和增加经济效益,选用外来优秀黑白花公牛(冻精)配种,这是提高当地黑白花 奶牛产奶量的有效方法. 2.5增加光照实践结果表明,在短日照季 节里,给奶牛人工补充光照,使自然光照与 人工补充光照总时间达到16小时,可提高奶牛的产奶量. 2.6保持奶牛卫生和运动锻炼经常给奶 牛刷拭,适当运动,每天上下午把奶牛各放 开一次,让奶牛运动3～3.5kin,会提高产奶量10%～15%. 2.7经常进行牛群整顿,做好良种培育要 坚持"选优去劣"原则,及时淘汰久配不孕, 生产性能低和年老体弱的母牛,并选出优秀后备母牛进行补充. 2.8做好奶牛防暑降温和防寒保暖工作综 上所述,提高奶牛产奶量的饲养措施和管理措施是多方面的,两者必须更好地配合,在 各项措施的应用上,要有选择性,灵活性, 做到恰当适用,有条不紊,要面对现实,力 争创新,只有这样,才能使奶牛保持高产,
关于奶牛的产前和产后管理奶牛的繁殖在奶牛的饲养中是非常重要的过程,因为没有奶牛的繁殖就没有牛奶,就没有新生牛的补充,就无法进行生产,奶牛的产前和产后管理,直接影响着奶牛的繁殖效率.下面分几个阶段前和产后管理 一,分娩的预兆 奶牛的预产期通常按280天计算。奶牛在分娩前后机体要发生一系列的变化，主要有下面几方面 ①骨盆的变化，母牛在怀孕后期，由于骨盆腔内的血管血流量增加，毛细血管的扩张， 部分血浆出血管壁，浸润周围的组织而使骨盆韧带松弛变软。当荐坐韧带变的非常松软，用手触摸似一团软组织感，且尾根两侧出现明显的塌陷现象，一般不超过24小时即可分娩。 ②外阴部的变化。母牛分娩前数天，阴唇逐渐肿胀阴唇上皮肤皱纹平展，质的变软， 阴道黏膜潮红，黏液由稠变稀，子宫栓软化从阴道排出，有时挂在阴户上。 ③乳房的变化。乳房在分娩前迅速发育，腺体充实。临产45天可挤出少量清亮胶样 液体，产前2——3天可挤出初乳，乳头变粗，表面光亮，有的母牛有滴奶现象。 ④体温的变化。在妊娠8——9个月时体温升到39摄氏度，但临产前约下降0.4---0.8 度，坚持每日清晨测温可以发现产期的到来。 ⑤精神的变化。母牛在临产时，由于子宫颈的高度扩张，子宫痛缩，开始出现阵痛现 象，母牛的食欲下降，表现出精神不安，时起时卧举尾频尿，回顾腹部，拱腰，后驱左右摆动，哞叫等。 二，分娩过程： 正常的奶牛分娩过程一般分为3个阶段！ 1、开口期。子宫纵形肌和环形肌开始间歇性收缩，并向子宫方向进行驱出运动，使 子宫劲完全开放，与阴道的界限消失。这时期的特点是只阵缩而不出现努责。此时，母 牛表现出精神变化。不安，时起时卧，来回走动而弓背抬尾，作排便姿势，哞叫。开口 期一般需要1——12小时。平均为6小时，出产母牛表现症状比经产母牛明显，时间较 长。 2、胎儿产出期：是指子宫颈完全开张至胎儿产出为止，特点是子宫肌发生更频繁有 力的阵缩，同时腹肌和痛肌也发生强烈收缩（努责），腹内压显著升高，这个时期的子 宫肌收缩期延长，松弛期缩短，弓背努责，经多次努责，从阴户口可见淡白或微黄色，半透明，膜上有少数细而直的血管，膜破裂后，流出黄色的液体，然后包囊胎儿蹄子的 羊膜囊部分的露出阴口在阵缩和努责的作用下，羊膜囊破裂流出白色混浊的羊水，整 个胎儿排出产道。这个阶段一般持续0.5——4小时。如羊膜破裂后半小时以上胎儿不 能自行产出，必须进行人工助产。 3胎衣排出期：是指从胎儿排出到胎衣排出为止这段时间。胎儿产出后，一般经6——12小时的间歇，收缩的间歇期较长，直至将胎衣完全排出。至此分娩过程结束。 牛的胎盘属于子叶型胎盘，母子胎盘之间的连接较为紧密，在收缩时子叶不易脱落。 因此胎衣排出时间很长，一般为2——8小时，如果12小时以后胎衣仍未排出，即为胎 衣不下，需及时采取措施。 三，助产 是指在自然分娩出现某种困难时人工帮助产出胎儿。奶牛的助产是及时处理奶牛难产。进行正确的产后处理以及预防产后奶牛炎症和犊牛健康的重要环节。分娩是母牛正常的生理过程，一般情况下，不需要助产而任期自然产出。但是在胎位不正。胎儿过大，母牛分娩乏力等自然分娩有一定困难的情况下，需进行必要的助产。
产后访视和产后42天健康检查 中国疾病预防控制中心李丽娟 一、概述 （一）意义 产后访视和产后 42 天健康检查具有很大的意义，它是孕产期保健的重要组成部分，可以促进母乳喂养，防治产褥感染及产后抑郁等，也是保障母婴安全、母婴健康的重要环节。 （二）产褥期产妇的生理变化 在产褥期产妇身体上各个系统都在发生变化，除乳房以外，均要恢复到未孕状态。 1 ．子宫 子宫要逐渐复原，宫底要下降。子宫的恢复主要表现在：它开始收缩变硬，逐渐缩小；产后 1 周耻骨联合上可触及宫底；但产后 10 天以后子宫即进入了盆腔，耻骨联合上再触不到宫底；产后 6 周，子宫可恢复到未孕时大小；即子宫要从分娩前的 1000 克逐渐恢复到未孕时的 50 克。 2 ．乳房 产褥期最重要的变化是乳房的变化，分娩以后乳房开始有乳汁分泌；要早吸吮、早开奶。吸吮刺激是使乳汁不断分泌的关键环节；坚持母乳喂养是给孩子最好的礼物。 3 ．内分泌 产褥期妇女内分泌的变化主要表现在：恢复月经和恢复排卵；在不哺乳的情况下产后 6 ～ 10 周可以恢复月经；产后 10 周左右能恢复排卵；在哺乳的情况下妇女月经恢复延迟，部分哺乳期妇女月经一直不来潮；一般情况下产后 4 ～ 6 个月可恢复排卵；大多数产后月经复潮前多有排卵，所以要注意避孕。 二、产后访视 （一）时间与对象 乡镇卫生院、村卫生室和社区卫生服务中心（站）在收到分娩医院转来的产妇分娩信息后，应于产后 3 ～7 天、产后 28 天分别到产妇家中进行产后访视 1 次，对产妇及新生儿同时访视，出现母婴异常情况适当增加访视次数或指导及时就医。
（二）访视流程 产后访视应遵循访视流程： 1. 访视前电话预约。 2. 社区访视人员应统一着装，佩带上岗证。 3. 按门铃或敲门、自我介绍、说明来访目的。 4. 进入产妇家，在接触母婴前，清洁双手。 5. 检查顺序：先检查新生儿后检查产妇。 （三）访视包 访视人员要携带访视包，访视必备物品包括血压计、听诊器、体温计、 75% 的酒精、酒精棉球、消毒棉签、塑料布、一次性消毒手套、婴儿秤、布兜、电筒等。附带物品有镊子、拆线剪、处方、新洁尔灭、母乳喂养指导的资料。生活用品包括一次性脚套、一次性臀垫。 （四）产后访视主要内容 产后访视主要内容包括以下几个方面： 1. 询问和了解母婴情况； 2. 观察母婴情况； 3. 母婴体格检查； 4. 异常情况的处理原则； 5. 提供保健指导； 6. 记录访视卡。 1．询问和了解母婴情况 首先要询问母婴情况，了解产妇分娩方式、产程是否顺利、有无难产经历、产后出血情况、孕产期有无合并症、并发症等，如果有合并症、并发症，了解其诊断及治疗经过。询问产妇目前情况，有没有头晕、疲乏等异常情况，同时询问哺乳的情况，乳汁量是否充足，再询问饮食、二便的情况。而后通过母亲要询问孩子的情况，包括孩子的喂养、大小便、睡眠、哭声等。另外要了解新生儿预防接种情况，如卡介苗和乙肝疫苗的接种情况。 询问时，要注意以下两个方面： 第一、询问前，需了解母子保健卡记录的内容，对于新生儿畸形和先天性缺陷等情况，询问时避免问及伤心问题，以免影响产妇情绪。第二，要面带微笑，给人以温暖的感觉，营造良好的氛围。 2 ．观察母婴情况 询问时观察产妇的精神状态、面色，同时要检查产妇的恶露情况，如恶露的颜色、量、有无异味；同时要观察母亲的哺乳姿势；而后要观察新生儿的一般情况，包括呼吸、皮肤颜色及孩子的吸奶情况。另外还要了解居住的环境状况，包括室温、湿度是否适宜、通风状况、室内用具是否清洁卫生、新生儿的衣被和尿布是否符合卫生要求等。 3 ．体格检查 （ 1 ）新生儿
奶牛产后常见疾病得防治 产后奶牛在产后7～10天阶段,每天要认真检查产后奶牛得体温、精神、采食、反刍、肢蹄、恶露颜色、乳房充盈度、瘤胃充盈度、子宫排泄物与粪便形态等情况并做好分析记录。要注意产后奶牛分娩后胎衣脱落排出得时间与子宫排出物得形态、颜色与气味等情况。正常得情况下产后奶牛一般在12～24小时以内就能自行排出胎衣。超过时间就应视为胎衣滞留,应及时采取相应得诊治措施,防止产后奶牛胎衣在体内长时间滞留。对于双胎、早产、难产、死胎、瘦弱、庝痛等得产后奶牛及时进行全身检查,及早诊疗,促进康复。体况评分:要求产后奶牛体况分值3、5～3、75范围以内。对于体况偏差得产后奶牛要加强饲养管理,促使体况达到标准要求。 1、每周进行一次产后奶牛酮病检测:对检测结果为3+得产后奶牛,须注射B族类维生素,灌服丙二醇等药物予以早期预防治疗; 2、预防低血钙、产后瘫痪、酮病等产后常见疾病:每1～3天抽血检测一次血钙水平与酮体、BHBA水平。根据实验室检测数据指标,采取相应预防措施。也可灌服以下配合预防药物:丙酸钙450～500g、氯化钾100g、硫酸镁220g、酵母200～300g、阿斯匹林粉45～50g、25度左右温水30～50L。其中钙制剂可以视情多灌服2～3次; 3、对产道拉伤与庝痛严重得产后奶牛:每2天用消毒液、凡士林、消炎粉等药物处理创面;肌肉注射镇痛消炎药缓解疼痛,消炎消肿; 4、预防产后奶牛胎衣滞留:可注射缩宫素促进胎衣排出。即在奶牛产后1、4、7小时分别注射40IU催产素,第二天如胎衣仍没有排出,
可再注射适量前列腺素促进胎衣排出。如果注射药物无效,就需要采用子宫冲洗注药得方法促使胎衣排出。具体方法如下:先用消毒药液将产后奶牛得外阴处清洗干净。用手臂将将已消毒过得透明塑料软管送入阴道,再通过子宫颈到达子宫低垂部后引导出子宫恶露。然后经软管注入5%～10%糖盐水500～1000ml溶液冲洗子宫,导净子宫内得存液后,再注入土霉素5g、利凡诺0、5g、生理盐水 500ml。每隔一天一次,直至滞留胎衣排出; 5、防治子宫炎:对感染子宫炎与子宫内膜炎得产后奶牛及产后30天子宫还没有正常复原得产后奶牛,可采取抗菌素进行子宫冲洗得治疗措施。对于严重感染得牛可以每隔3天再连续冲洗3次子宫得治疗办法。常用于治疗子宫内膜炎得药物有抗菌消炎、激素、防腐类等药物。可用40℃左右得0、1%～0、3%高锰酸钾200～300ml冲洗子宫,同时可用手经直肠按摩提压子宫,促使药液能将子宫冲排干净。尔后再取青霉素160万U与链霉素100万U溶于无菌水100ml,注入子宫消炎。或取土霉素粉2～3g溶于100ml生理盐水中后注入子宫消炎。对病情较重、子宫肥厚、不断排出脓性分泌物,已转化成慢性子宫内膜炎得产后奶牛,可肌注乙烯雌酚20mg或脑垂体后叶素100U促使子宫收缩,进行配合治疗。产后奶牛冲洗子宫一般每2天一次,一个疗程视情冲洗子宫3～5次。当产后奶牛体温≥39、5℃,采食、反刍减少、精神沉郁出现全身症状时,要及时做系统得诊查并且采取全身治疗措施;